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首页> 外文期刊>Journal of biochemical and molecular toxicology >Diallyl sulfide ameliorates carbon tetrachloride-induced hepatotoxicity in rats via suppressing stress-activated MAPK signaling pathways
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Diallyl sulfide ameliorates carbon tetrachloride-induced hepatotoxicity in rats via suppressing stress-activated MAPK signaling pathways

机译：通过抑制应力激活的MAPK信号通路，二烯丙基硫化物在大鼠中改变了大鼠四氯化物诱导的肝毒性

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摘要

The underlined effects of diallyl sulfide (DAS) against CCL4-induced oxidative, inflammatory, and apoptotic acute hepatic damage were assessed. Administration of DAS (50, 100, and 200 mg/kg) along with CCL4 effectively mitigated serum aspartate aminotransferase, alanine aminotransferase activities, MDA, TNF-alpha, IL-1 beta, and MCP-1 levels, as well as significantly restored HO-1, GSH levels and SOD activity in liver tissues compared with those in rats treated with CCL4. Moreover, DAS inhibited CCL4-induced increase of liver NF-kappa B (p65), Bax, p38 MAPK, and JNK protein expression. In addition, DAS accelerated protein expression of Nrf2 and Bcl-2. The hepatoprotective properties of DAS were further confirmed by the reduced severity of hepatic damage as demonstrated by histopathological findings. In conclusion, DAS achieved its protective potential against CCL4-induced hepatotoxicity through antiapoptotic activity, as well as the synchronized modulation of NF-kappa B and Nrf2 for the favor of antioxidant/anti-inflammatory effects via suppression of the upstream stress-activated MAPKs pathways.
机译：评估二烯丙基硫化物（DAS）对CCL4诱导的氧化，炎症和凋亡急性肝损伤的带下划线的效果。将DAS（50,100和200mg / kg）与CCL4一起施用有效减轻血清天冬氨酸氨基转移酶，丙氨酸氨基转移酶活性，MDA，TNF-α，IL-1β和MCP-1水平，以及显着恢复与用CCl4处理的大鼠相比，肝组织中的-1，GSH水平和SOD活性。此外，DAS抑制CCL4诱导的肝脏NF-κB（P65），BAX，P38 MAPK和JNK蛋白表达增加。此外，DAS加速NRF2和BCL-2的蛋白表达。通过组织病理学发现证明的肝损伤的严重程度，进一步证实了DA的肝保护性能。总之，DAS通过抗曝气活性实现了对CCL4诱导的肝毒性的保护潜力，以及通过抑制上游应力激活的MAPKS途径来支持抗氧化/抗炎作用的NF-Kappa B和NRF2的同步调制。

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