Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats

Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effec...
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Autor*in:	Wang, Xianbin [verfasserIn] Wang, Ting [verfasserIn] Pan, Tingting [verfasserIn] Huang, Mei [verfasserIn] Ren, Weihua [verfasserIn] Xu, Geliang [verfasserIn] Amin, Hatem K. [verfasserIn] Kassab, Rami B. [verfasserIn] Abdel Moneim, Ahmed E. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Cadmium Oxidative stress Nuclear factor erythroid 2-related factor 2 Inflammation Apoptosis Liver

Übergeordnetes Werk:	Enthalten in: Environmental science and pollution research - Berlin : Springer, 1994, 27(2019), 6 vom: 20. Dez., Seite 5981-5992
Übergeordnetes Werk:	volume:27 ; year:2019 ; number:6 ; day:20 ; month:12 ; pages:5981-5992

Links:	Volltext

DOI / URN:	10.1007/s11356-019-07117-3

Katalog-ID:	SPR018893988

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245	1	0	\|a Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats
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520			\|a Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract
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700	1		\|a Ren, Weihua \|e verfasserin \|4 aut
700	1		\|a Xu, Geliang \|e verfasserin \|4 aut
700	1		\|a Amin, Hatem K. \|e verfasserin \|4 aut
700	1		\|a Kassab, Rami B. \|e verfasserin \|4 aut
700	1		\|a Abdel Moneim, Ahmed E. \|e verfasserin \|4 aut
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Indexfelder

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allfields	10.1007/s11356-019-07117-3 doi (DE-627)SPR018893988 (SPR)s11356-019-07117-3-e DE-627 ger DE-627 rakwb eng 333.7 690 ASE 43.00 bkl 43.50 bkl 58.50 bkl Wang, Xianbin verfasserin aut Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract Cadmium (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Nuclear factor erythroid 2-related factor 2 (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Wang, Ting verfasserin aut Pan, Tingting verfasserin aut Huang, Mei verfasserin aut Ren, Weihua verfasserin aut Xu, Geliang verfasserin aut Amin, Hatem K. verfasserin aut Kassab, Rami B. verfasserin aut Abdel Moneim, Ahmed E. verfasserin aut Enthalten in Environmental science and pollution research Berlin : Springer, 1994 27(2019), 6 vom: 20. Dez., Seite 5981-5992 (DE-627)320517926 (DE-600)2014192-0 1614-7499 nnns volume:27 year:2019 number:6 day:20 month:12 pages:5981-5992 https://dx.doi.org/10.1007/s11356-019-07117-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OPC-GGO SSG-OPC-ASE GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2360 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 43.00 ASE 43.50 ASE 58.50 ASE AR 27 2019 6 20 12 5981-5992
spelling	10.1007/s11356-019-07117-3 doi (DE-627)SPR018893988 (SPR)s11356-019-07117-3-e DE-627 ger DE-627 rakwb eng 333.7 690 ASE 43.00 bkl 43.50 bkl 58.50 bkl Wang, Xianbin verfasserin aut Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract Cadmium (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Nuclear factor erythroid 2-related factor 2 (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Wang, Ting verfasserin aut Pan, Tingting verfasserin aut Huang, Mei verfasserin aut Ren, Weihua verfasserin aut Xu, Geliang verfasserin aut Amin, Hatem K. verfasserin aut Kassab, Rami B. verfasserin aut Abdel Moneim, Ahmed E. verfasserin aut Enthalten in Environmental science and pollution research Berlin : Springer, 1994 27(2019), 6 vom: 20. Dez., Seite 5981-5992 (DE-627)320517926 (DE-600)2014192-0 1614-7499 nnns volume:27 year:2019 number:6 day:20 month:12 pages:5981-5992 https://dx.doi.org/10.1007/s11356-019-07117-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OPC-GGO SSG-OPC-ASE GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2360 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 43.00 ASE 43.50 ASE 58.50 ASE AR 27 2019 6 20 12 5981-5992
allfields_unstemmed	10.1007/s11356-019-07117-3 doi (DE-627)SPR018893988 (SPR)s11356-019-07117-3-e DE-627 ger DE-627 rakwb eng 333.7 690 ASE 43.00 bkl 43.50 bkl 58.50 bkl Wang, Xianbin verfasserin aut Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract Cadmium (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Nuclear factor erythroid 2-related factor 2 (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Wang, Ting verfasserin aut Pan, Tingting verfasserin aut Huang, Mei verfasserin aut Ren, Weihua verfasserin aut Xu, Geliang verfasserin aut Amin, Hatem K. verfasserin aut Kassab, Rami B. verfasserin aut Abdel Moneim, Ahmed E. verfasserin aut Enthalten in Environmental science and pollution research Berlin : Springer, 1994 27(2019), 6 vom: 20. Dez., Seite 5981-5992 (DE-627)320517926 (DE-600)2014192-0 1614-7499 nnns volume:27 year:2019 number:6 day:20 month:12 pages:5981-5992 https://dx.doi.org/10.1007/s11356-019-07117-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OPC-GGO SSG-OPC-ASE GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2360 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 43.00 ASE 43.50 ASE 58.50 ASE AR 27 2019 6 20 12 5981-5992
allfieldsGer	10.1007/s11356-019-07117-3 doi (DE-627)SPR018893988 (SPR)s11356-019-07117-3-e DE-627 ger DE-627 rakwb eng 333.7 690 ASE 43.00 bkl 43.50 bkl 58.50 bkl Wang, Xianbin verfasserin aut Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract Cadmium (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Nuclear factor erythroid 2-related factor 2 (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Wang, Ting verfasserin aut Pan, Tingting verfasserin aut Huang, Mei verfasserin aut Ren, Weihua verfasserin aut Xu, Geliang verfasserin aut Amin, Hatem K. verfasserin aut Kassab, Rami B. verfasserin aut Abdel Moneim, Ahmed E. verfasserin aut Enthalten in Environmental science and pollution research Berlin : Springer, 1994 27(2019), 6 vom: 20. Dez., Seite 5981-5992 (DE-627)320517926 (DE-600)2014192-0 1614-7499 nnns volume:27 year:2019 number:6 day:20 month:12 pages:5981-5992 https://dx.doi.org/10.1007/s11356-019-07117-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OPC-GGO SSG-OPC-ASE GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2360 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 43.00 ASE 43.50 ASE 58.50 ASE AR 27 2019 6 20 12 5981-5992
allfieldsSound	10.1007/s11356-019-07117-3 doi (DE-627)SPR018893988 (SPR)s11356-019-07117-3-e DE-627 ger DE-627 rakwb eng 333.7 690 ASE 43.00 bkl 43.50 bkl 58.50 bkl Wang, Xianbin verfasserin aut Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract Cadmium (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Nuclear factor erythroid 2-related factor 2 (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Wang, Ting verfasserin aut Pan, Tingting verfasserin aut Huang, Mei verfasserin aut Ren, Weihua verfasserin aut Xu, Geliang verfasserin aut Amin, Hatem K. verfasserin aut Kassab, Rami B. verfasserin aut Abdel Moneim, Ahmed E. verfasserin aut Enthalten in Environmental science and pollution research Berlin : Springer, 1994 27(2019), 6 vom: 20. Dez., Seite 5981-5992 (DE-627)320517926 (DE-600)2014192-0 1614-7499 nnns volume:27 year:2019 number:6 day:20 month:12 pages:5981-5992 https://dx.doi.org/10.1007/s11356-019-07117-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OPC-GGO SSG-OPC-ASE GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2360 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 43.00 ASE 43.50 ASE 58.50 ASE AR 27 2019 6 20 12 5981-5992
language	English
source	Enthalten in Environmental science and pollution research 27(2019), 6 vom: 20. Dez., Seite 5981-5992 volume:27 year:2019 number:6 day:20 month:12 pages:5981-5992
sourceStr	Enthalten in Environmental science and pollution research 27(2019), 6 vom: 20. Dez., Seite 5981-5992 volume:27 year:2019 number:6 day:20 month:12 pages:5981-5992
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Cadmium Oxidative stress Nuclear factor erythroid 2-related factor 2 Inflammation Apoptosis Liver
dewey-raw	333.7
isfreeaccess_bool	false
container_title	Environmental science and pollution research
authorswithroles_txt_mv	Wang, Xianbin @@aut@@ Wang, Ting @@aut@@ Pan, Tingting @@aut@@ Huang, Mei @@aut@@ Ren, Weihua @@aut@@ Xu, Geliang @@aut@@ Amin, Hatem K. @@aut@@ Kassab, Rami B. @@aut@@ Abdel Moneim, Ahmed E. @@aut@@
publishDateDaySort_date	2019-12-20T00:00:00Z
hierarchy_top_id	320517926
dewey-sort	3333.7
id	SPR018893988
language_de	englisch
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Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. 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author	Wang, Xianbin
spellingShingle	Wang, Xianbin ddc 333.7 bkl 43.00 bkl 43.50 bkl 58.50 misc Cadmium misc Oxidative stress misc Nuclear factor erythroid 2-related factor 2 misc Inflammation misc Apoptosis misc Liver Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats
authorStr	Wang, Xianbin
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illustrated	Not Illustrated
issn	1614-7499
topic_title	333.7 690 ASE 43.00 bkl 43.50 bkl 58.50 bkl Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats Cadmium (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Nuclear factor erythroid 2-related factor 2 (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Liver (dpeaa)DE-He213
topic	ddc 333.7 bkl 43.00 bkl 43.50 bkl 58.50 misc Cadmium misc Oxidative stress misc Nuclear factor erythroid 2-related factor 2 misc Inflammation misc Apoptosis misc Liver
topic_unstemmed	ddc 333.7 bkl 43.00 bkl 43.50 bkl 58.50 misc Cadmium misc Oxidative stress misc Nuclear factor erythroid 2-related factor 2 misc Inflammation misc Apoptosis misc Liver
topic_browse	ddc 333.7 bkl 43.00 bkl 43.50 bkl 58.50 misc Cadmium misc Oxidative stress misc Nuclear factor erythroid 2-related factor 2 misc Inflammation misc Apoptosis misc Liver
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
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hierarchy_parent_title	Environmental science and pollution research
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dewey-tens	330 - Economics 690 - Building & construction
hierarchy_top_title	Environmental science and pollution research
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title	Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats
ctrlnum	(DE-627)SPR018893988 (SPR)s11356-019-07117-3-e
title_full	Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats
author_sort	Wang, Xianbin
journal	Environmental science and pollution research
journalStr	Environmental science and pollution research
lang_code	eng
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dewey-hundreds	300 - Social sciences 600 - Technology
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container_start_page	5981
author_browse	Wang, Xianbin Wang, Ting Pan, Tingting Huang, Mei Ren, Weihua Xu, Geliang Amin, Hatem K. Kassab, Rami B. Abdel Moneim, Ahmed E.
container_volume	27
class	333.7 690 ASE 43.00 bkl 43.50 bkl 58.50 bkl
format_se	Elektronische Aufsätze
author-letter	Wang, Xianbin
doi_str_mv	10.1007/s11356-019-07117-3
dewey-full	333.7 690
author2-role	verfasserin
title_sort	senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats
title_auth	Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats
abstract	Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract
abstractGer	Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract
abstract_unstemmed	Abstract Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride ($ CdCl_{2} $)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), $ CdCl_{2} $ (0.6 mg/kg), and SAE + $ CdCl_{2} $, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before $ CdCl_{2} $ exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by $ CdCl_{2} $ exposure. SAE can be used as a promising protective agent against $ CdCl_{2} $-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract
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container_issue	6
title_short	Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats
url	https://dx.doi.org/10.1007/s11356-019-07117-3
remote_bool	true
author2	Wang, Ting Pan, Tingting Huang, Mei Ren, Weihua Xu, Geliang Amin, Hatem K. Kassab, Rami B. Abdel Moneim, Ahmed E.
author2Str	Wang, Ting Pan, Tingting Huang, Mei Ren, Weihua Xu, Geliang Amin, Hatem K. Kassab, Rami B. Abdel Moneim, Ahmed E.
ppnlink	320517926
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doi_str	10.1007/s11356-019-07117-3
up_date	2024-07-03T22:59:44.770Z
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Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats

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