Exercise antagonizes cadmium-caused liver and intestinal injury in mice via Nrf2 and TLR2/NF-κB signalling pathway DOI Creative Commons
Ding Zhang, Jiayi Liu, Jingru Liu

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2025, Номер 294, С. 118100 - 118100

Опубликована: Апрель 1, 2025

Cadmium (Cd) causes a health risk to humans and animals. Exercise can prevent treat variety of diseases, but the effect mechanism exercise on cadmium poisoning are still unclear. The present research aims investigate antagonistic impacts enterotoxicity hepatotoxicity caused by Cd. results indicated that exercise, both before during Cd exposure, reduce pathological damages in liver duodenum mice, suppressing expression levels IL-1β, IL-6 TNF-α genes. In mice exposed Cd, significantly decreased blood ALT AST levels, alleviating oxidative stress reducing MDA synthesis enhancing SOD GSH-PX activities. inhibited nuclear damage hepatocyte apoptosis increasing Bcl-2 protein preventing release pro-apoptotic proteins such as caspase-3, Cytc, Bax, caspase-8and cleaved-caspase-3. or exposure increase gene HO-1, NQO-1 Nrf2 These findings suggested signaling pathway may have contributed exercise-induced partial attenuation Cd-induced hepatic injury. also promoted occludin Cd-exposed decreasing structural inflammatory cell infiltration induced NF-κB TLR2 were elevated However, mitigated Cd-intoxicated suggesting protective effects intestinal tract be mediated through modulation NF-κB/TLR2 pathway. conclusion, this study elucidated against injury mice. mechanisms partially realized regulation pathways.

Язык: Английский

Exercise antagonizes cadmium-caused liver and intestinal injury in mice via Nrf2 and TLR2/NF-κB signalling pathway DOI Creative Commons
Ding Zhang, Jiayi Liu, Jingru Liu

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2025, Номер 294, С. 118100 - 118100

Опубликована: Апрель 1, 2025

Cadmium (Cd) causes a health risk to humans and animals. Exercise can prevent treat variety of diseases, but the effect mechanism exercise on cadmium poisoning are still unclear. The present research aims investigate antagonistic impacts enterotoxicity hepatotoxicity caused by Cd. results indicated that exercise, both before during Cd exposure, reduce pathological damages in liver duodenum mice, suppressing expression levels IL-1β, IL-6 TNF-α genes. In mice exposed Cd, significantly decreased blood ALT AST levels, alleviating oxidative stress reducing MDA synthesis enhancing SOD GSH-PX activities. inhibited nuclear damage hepatocyte apoptosis increasing Bcl-2 protein preventing release pro-apoptotic proteins such as caspase-3, Cytc, Bax, caspase-8and cleaved-caspase-3. or exposure increase gene HO-1, NQO-1 Nrf2 These findings suggested signaling pathway may have contributed exercise-induced partial attenuation Cd-induced hepatic injury. also promoted occludin Cd-exposed decreasing structural inflammatory cell infiltration induced NF-κB TLR2 were elevated However, mitigated Cd-intoxicated suggesting protective effects intestinal tract be mediated through modulation NF-κB/TLR2 pathway. conclusion, this study elucidated against injury mice. mechanisms partially realized regulation pathways.

Язык: Английский

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