Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation

Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were construc...
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Autor*in:	Hao Yang [verfasserIn] Xiyuan Ping [verfasserIn] Yilei Cui [verfasserIn] Sifan Zheng [verfasserIn] Xingchao Shentu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Cataract UVB Autophagy Apoptosis HLECs Oxidative stress

Übergeordnetes Werk:	In: Advances in Ophthalmology Practice and Research - Elsevier, 2022, 3(2023), 1, Seite 15-22
Übergeordnetes Werk:	volume:3 ; year:2023 ; number:1 ; pages:15-22

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.aopr.2022.09.002

Katalog-ID:	DOAJ081199570

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520			\|a Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC).
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allfields	10.1016/j.aopr.2022.09.002 doi (DE-627)DOAJ081199570 (DE-599)DOAJ65e199dfc8674ff5aaba6d7f438c21c5 DE-627 ger DE-627 rakwb eng RE1-994 Hao Yang verfasserin aut Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC). Cataract UVB Autophagy Apoptosis HLECs Oxidative stress Ophthalmology Xiyuan Ping verfasserin aut Yilei Cui verfasserin aut Sifan Zheng verfasserin aut Xingchao Shentu verfasserin aut In Advances in Ophthalmology Practice and Research Elsevier, 2022 3(2023), 1, Seite 15-22 (DE-627)1789916518 26673762 nnns volume:3 year:2023 number:1 pages:15-22 https://doi.org/10.1016/j.aopr.2022.09.002 kostenfrei https://doaj.org/article/65e199dfc8674ff5aaba6d7f438c21c5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2667376222000701 kostenfrei https://doaj.org/toc/2667-3762 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2023 1 15-22
spelling	10.1016/j.aopr.2022.09.002 doi (DE-627)DOAJ081199570 (DE-599)DOAJ65e199dfc8674ff5aaba6d7f438c21c5 DE-627 ger DE-627 rakwb eng RE1-994 Hao Yang verfasserin aut Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC). Cataract UVB Autophagy Apoptosis HLECs Oxidative stress Ophthalmology Xiyuan Ping verfasserin aut Yilei Cui verfasserin aut Sifan Zheng verfasserin aut Xingchao Shentu verfasserin aut In Advances in Ophthalmology Practice and Research Elsevier, 2022 3(2023), 1, Seite 15-22 (DE-627)1789916518 26673762 nnns volume:3 year:2023 number:1 pages:15-22 https://doi.org/10.1016/j.aopr.2022.09.002 kostenfrei https://doaj.org/article/65e199dfc8674ff5aaba6d7f438c21c5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2667376222000701 kostenfrei https://doaj.org/toc/2667-3762 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2023 1 15-22
allfields_unstemmed	10.1016/j.aopr.2022.09.002 doi (DE-627)DOAJ081199570 (DE-599)DOAJ65e199dfc8674ff5aaba6d7f438c21c5 DE-627 ger DE-627 rakwb eng RE1-994 Hao Yang verfasserin aut Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC). Cataract UVB Autophagy Apoptosis HLECs Oxidative stress Ophthalmology Xiyuan Ping verfasserin aut Yilei Cui verfasserin aut Sifan Zheng verfasserin aut Xingchao Shentu verfasserin aut In Advances in Ophthalmology Practice and Research Elsevier, 2022 3(2023), 1, Seite 15-22 (DE-627)1789916518 26673762 nnns volume:3 year:2023 number:1 pages:15-22 https://doi.org/10.1016/j.aopr.2022.09.002 kostenfrei https://doaj.org/article/65e199dfc8674ff5aaba6d7f438c21c5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2667376222000701 kostenfrei https://doaj.org/toc/2667-3762 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2023 1 15-22
allfieldsGer	10.1016/j.aopr.2022.09.002 doi (DE-627)DOAJ081199570 (DE-599)DOAJ65e199dfc8674ff5aaba6d7f438c21c5 DE-627 ger DE-627 rakwb eng RE1-994 Hao Yang verfasserin aut Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC). Cataract UVB Autophagy Apoptosis HLECs Oxidative stress Ophthalmology Xiyuan Ping verfasserin aut Yilei Cui verfasserin aut Sifan Zheng verfasserin aut Xingchao Shentu verfasserin aut In Advances in Ophthalmology Practice and Research Elsevier, 2022 3(2023), 1, Seite 15-22 (DE-627)1789916518 26673762 nnns volume:3 year:2023 number:1 pages:15-22 https://doi.org/10.1016/j.aopr.2022.09.002 kostenfrei https://doaj.org/article/65e199dfc8674ff5aaba6d7f438c21c5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2667376222000701 kostenfrei https://doaj.org/toc/2667-3762 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2023 1 15-22
allfieldsSound	10.1016/j.aopr.2022.09.002 doi (DE-627)DOAJ081199570 (DE-599)DOAJ65e199dfc8674ff5aaba6d7f438c21c5 DE-627 ger DE-627 rakwb eng RE1-994 Hao Yang verfasserin aut Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC). Cataract UVB Autophagy Apoptosis HLECs Oxidative stress Ophthalmology Xiyuan Ping verfasserin aut Yilei Cui verfasserin aut Sifan Zheng verfasserin aut Xingchao Shentu verfasserin aut In Advances in Ophthalmology Practice and Research Elsevier, 2022 3(2023), 1, Seite 15-22 (DE-627)1789916518 26673762 nnns volume:3 year:2023 number:1 pages:15-22 https://doi.org/10.1016/j.aopr.2022.09.002 kostenfrei https://doaj.org/article/65e199dfc8674ff5aaba6d7f438c21c5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2667376222000701 kostenfrei https://doaj.org/toc/2667-3762 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2023 1 15-22
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callnumber-first	R - Medicine
author	Hao Yang
spellingShingle	Hao Yang misc RE1-994 misc Cataract misc UVB misc Autophagy misc Apoptosis misc HLECs misc Oxidative stress misc Ophthalmology Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation
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topic_title	RE1-994 Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation Cataract UVB Autophagy Apoptosis HLECs Oxidative stress
topic	misc RE1-994 misc Cataract misc UVB misc Autophagy misc Apoptosis misc HLECs misc Oxidative stress misc Ophthalmology
topic_unstemmed	misc RE1-994 misc Cataract misc UVB misc Autophagy misc Apoptosis misc HLECs misc Oxidative stress misc Ophthalmology
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title	Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation
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title_full	Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation
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title_sort	role of rapamycin and 3-ma in oxidative damage of hlecs caused by two doses of uvb radiation
callnumber	RE1-994
title_auth	Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation
abstract	Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC).
abstractGer	Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC).
abstract_unstemmed	Background: This study compared the role of autophagy regulators Rapamycin and 3-MA in oxidative damage and apoptosis of human lens epithelial cells (HLECs) caused by two doses of Ultraviolet Radiation B (UVB). Methods: HLECs were irradiated with UVB, and two doses of UVB damage models were constructed. After treatment with autophagy regulators, cell damage tests such as CCK-8, LDH activity, and Ros detection were performed. Western blotting was used to detect the levels of autophagy-related proteins and apoptosis-related proteins. Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA leve of secondary antioxidant enzymes.Flow cytometry was used to examine cell viability and apoptosis. Finally, the proportion of autophagy and apoptosis was observed by electron microscope. Results: Autophagy inhibitor 3-MA promoted oxidative damage and apoptosis of HLECs at low doses of UVB (5 mJ/cm2), which corresponds to 1.3 h of exposure to sunlight in human eyes. Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. It provides new ideas for reducing oxidative damage and apoptosis of HLECs to prevent or delay the progression of age-related cataract (ARC).
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title_short	Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation
url	https://doi.org/10.1016/j.aopr.2022.09.002 https://doaj.org/article/65e199dfc8674ff5aaba6d7f438c21c5 http://www.sciencedirect.com/science/article/pii/S2667376222000701 https://doaj.org/toc/2667-3762
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Under the high dose of UVB (50mJ/cm2), which is equivalent to 13 h of exposure to sunlight in human eyes, the autophagy inducer Rapamycin caused more extensive oxidative damage and apoptosis of HLECs. 3-MA was able to reduce this damage, indicating that moderate autophagy is necessary for HLECs to cope with mild oxidative stress. For high dose UVB-induced oxidative stress, the use of 3-MA inhibiting autophagy is more beneficial to reduce cell damage and apoptosis. The mechanisms include degradation of damaged organelles, regulation of the expression of antioxidant enzymes HO-1, NQO1, GCS and regulation of apoptosis-related proteins. Conclusions: Autophagy played different roles in HLECs oxidative stress induced by two doses of UVB. 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Role of Rapamycin and 3-MA in oxidative damage of HLECs caused by two doses of UVB radiation

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