<i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect

To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i&...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Seon Kyeong Park [verfasserIn] Jin Yong Kang [verfasserIn] Jong Min Kim [verfasserIn] Hyun-Jin Kim [verfasserIn] Ho Jin Heo [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	PM antioxidant anti-inflammation mitochondrial function cognition

Übergeordnetes Werk:	In: Marine Drugs - MDPI AG, 2005, 19(2021), 3, p 131
Übergeordnetes Werk:	volume:19 ; year:2021 ; number:3, p 131

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/md19030131

Katalog-ID:	DOAJ032790929

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allfields	10.3390/md19030131 doi (DE-627)DOAJ032790929 (DE-599)DOAJ61db6c5064704a7098f0dfd59af70d66 DE-627 ger DE-627 rakwb eng QH301-705.5 Seon Kyeong Park verfasserin aut <i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM<sub<2.5</sub<-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol. <i<Ecklonia cava</i< PM<sub<2.5</sub< antioxidant anti-inflammation mitochondrial function cognition Biology (General) Jin Yong Kang verfasserin aut Jong Min Kim verfasserin aut Hyun-Jin Kim verfasserin aut Ho Jin Heo verfasserin aut In Marine Drugs MDPI AG, 2005 19(2021), 3, p 131 (DE-627)477992420 (DE-600)2175190-0 16603397 nnns volume:19 year:2021 number:3, p 131 https://doi.org/10.3390/md19030131 kostenfrei https://doaj.org/article/61db6c5064704a7098f0dfd59af70d66 kostenfrei https://www.mdpi.com/1660-3397/19/3/131 kostenfrei https://doaj.org/toc/1660-3397 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_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_381 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2147 GBV_ILN_2148 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 19 2021 3, p 131
spelling	10.3390/md19030131 doi (DE-627)DOAJ032790929 (DE-599)DOAJ61db6c5064704a7098f0dfd59af70d66 DE-627 ger DE-627 rakwb eng QH301-705.5 Seon Kyeong Park verfasserin aut <i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM<sub<2.5</sub<-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol. <i<Ecklonia cava</i< PM<sub<2.5</sub< antioxidant anti-inflammation mitochondrial function cognition Biology (General) Jin Yong Kang verfasserin aut Jong Min Kim verfasserin aut Hyun-Jin Kim verfasserin aut Ho Jin Heo verfasserin aut In Marine Drugs MDPI AG, 2005 19(2021), 3, p 131 (DE-627)477992420 (DE-600)2175190-0 16603397 nnns volume:19 year:2021 number:3, p 131 https://doi.org/10.3390/md19030131 kostenfrei https://doaj.org/article/61db6c5064704a7098f0dfd59af70d66 kostenfrei https://www.mdpi.com/1660-3397/19/3/131 kostenfrei https://doaj.org/toc/1660-3397 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_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_381 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2147 GBV_ILN_2148 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 19 2021 3, p 131
allfields_unstemmed	10.3390/md19030131 doi (DE-627)DOAJ032790929 (DE-599)DOAJ61db6c5064704a7098f0dfd59af70d66 DE-627 ger DE-627 rakwb eng QH301-705.5 Seon Kyeong Park verfasserin aut <i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM<sub<2.5</sub<-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol. <i<Ecklonia cava</i< PM<sub<2.5</sub< antioxidant anti-inflammation mitochondrial function cognition Biology (General) Jin Yong Kang verfasserin aut Jong Min Kim verfasserin aut Hyun-Jin Kim verfasserin aut Ho Jin Heo verfasserin aut In Marine Drugs MDPI AG, 2005 19(2021), 3, p 131 (DE-627)477992420 (DE-600)2175190-0 16603397 nnns volume:19 year:2021 number:3, p 131 https://doi.org/10.3390/md19030131 kostenfrei https://doaj.org/article/61db6c5064704a7098f0dfd59af70d66 kostenfrei https://www.mdpi.com/1660-3397/19/3/131 kostenfrei https://doaj.org/toc/1660-3397 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_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_381 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2147 GBV_ILN_2148 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 19 2021 3, p 131
allfieldsGer	10.3390/md19030131 doi (DE-627)DOAJ032790929 (DE-599)DOAJ61db6c5064704a7098f0dfd59af70d66 DE-627 ger DE-627 rakwb eng QH301-705.5 Seon Kyeong Park verfasserin aut <i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM<sub<2.5</sub<-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol. <i<Ecklonia cava</i< PM<sub<2.5</sub< antioxidant anti-inflammation mitochondrial function cognition Biology (General) Jin Yong Kang verfasserin aut Jong Min Kim verfasserin aut Hyun-Jin Kim verfasserin aut Ho Jin Heo verfasserin aut In Marine Drugs MDPI AG, 2005 19(2021), 3, p 131 (DE-627)477992420 (DE-600)2175190-0 16603397 nnns volume:19 year:2021 number:3, p 131 https://doi.org/10.3390/md19030131 kostenfrei https://doaj.org/article/61db6c5064704a7098f0dfd59af70d66 kostenfrei https://www.mdpi.com/1660-3397/19/3/131 kostenfrei https://doaj.org/toc/1660-3397 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_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_381 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2147 GBV_ILN_2148 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 19 2021 3, p 131
allfieldsSound	10.3390/md19030131 doi (DE-627)DOAJ032790929 (DE-599)DOAJ61db6c5064704a7098f0dfd59af70d66 DE-627 ger DE-627 rakwb eng QH301-705.5 Seon Kyeong Park verfasserin aut <i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM<sub<2.5</sub<-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol. <i<Ecklonia cava</i< PM<sub<2.5</sub< antioxidant anti-inflammation mitochondrial function cognition Biology (General) Jin Yong Kang verfasserin aut Jong Min Kim verfasserin aut Hyun-Jin Kim verfasserin aut Ho Jin Heo verfasserin aut In Marine Drugs MDPI AG, 2005 19(2021), 3, p 131 (DE-627)477992420 (DE-600)2175190-0 16603397 nnns volume:19 year:2021 number:3, p 131 https://doi.org/10.3390/md19030131 kostenfrei https://doaj.org/article/61db6c5064704a7098f0dfd59af70d66 kostenfrei https://www.mdpi.com/1660-3397/19/3/131 kostenfrei https://doaj.org/toc/1660-3397 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_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_381 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2147 GBV_ILN_2148 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 19 2021 3, p 131
language	English
source	In Marine Drugs 19(2021), 3, p 131 volume:19 year:2021 number:3, p 131
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spellingShingle	Seon Kyeong Park misc QH301-705.5 misc <i<Ecklonia cava</i< misc PM<sub<2.5</sub< misc antioxidant misc anti-inflammation misc mitochondrial function misc cognition misc Biology (General) <i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect
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title_sort	<i<ecklonia cava</i< attenuates pm<sub<2.5</sub<-induced cognitive decline through mitochondrial activation and anti-inflammatory effect
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title_auth	<i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect
abstract	To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM<sub<2.5</sub<-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol.
abstractGer	To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM<sub<2.5</sub<-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol.
abstract_unstemmed	To evaluate the effects of <i<Ecklonia cava</i< (<i<E. cava</i<) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM<sub<2.5</sub<). The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM<sub<2.5</sub<-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol.
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title_short	<i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect
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The intake of water extract from <i<E. cava</i< (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM<sub<2.5</sub< exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM<sub<2.5</sub<-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). 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<i<Ecklonia cava</i< Attenuates PM<sub<2.5</sub<-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect

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