虫草素对四氯化碳所致小鼠急性肝损伤的保护作用

本文探究蛹虫草活性成分虫草素对四氯化碳（CCl₄）造成的小鼠急性肝损伤的保护作用及其分子机制。首先建立四氯化碳致小鼠急性肝损伤的动物模型,通过检测血清生化指标、肝功指标的变化及HE染色观察组织切片病理的病变情况,评价虫草素的保肝效果,进一步通过Western blot检测虫草素能否通过激活Nrf-2/Keap1信号通路及其下游抗氧化因子（HO-1、NQO-1）的表达来提高机体抗氧化损伤能力以及抑制炎症因子（TNFα、TNFβ、IL-6、IL-10）的表达。对比模型组结果显示,虫草素能极显著降低（P<0.01）小鼠血清中ALT、AST及肝脏中MDA水平,并能极显著提高肝脏中SOD水平（P<0.01）;HE染色结果显示虫草素能有效降低改善受损肝组织中的炎细胞浸润及纤维组织增生;Western blot结果表明虫草素能够通过激活Nrf-2信号通路,促进下游抗氧化因子及抗炎因子的表达,从而降低炎症反应。虫草素对CCl₄致小鼠急性肝损伤具有一定的保护作用,其机制与Nrf-2信号通路相关,实验结果为后续蛹虫草及虫草素的开发应用奠定基础。

Protective effects of cordycepin on CCl_4 induced acute liver injury in mice

The protective effect of cordycepin on acute liver injury induced by carbon tetrachloride (CCl₄) and its molecular mechanism were investigated. An animal model of acute liver injury induced by carbon tetrachloride in mice was established. The hepatoprotective effect of cordycepin was evaluated by detecting the changes of serum biochemical parameters and liver function indexes and observing the pathological changes of tissue sections via HE staining. Western blot analysis was used to study whether cordycepin could increase the body’s ability to resist oxidative damage and inhibit inflammatory factors (TNF-α, TNF-β, IL-6, IL-10) by activating the Nrf-2/Keap1 signaling pathway and expression of its downstream antioxidant factors (HO-1, NQO-1). In comparison with model group, cordycepin can significantly decrease the level (P<0.01) of serum ALT, AST and MDA and significantly increase SOD levels (P<0.01) in the liver. HE staining showed cordycepin could effectively reduce inflammatory cell infiltration and fibrous tissue proliferation in damaged liver tissue. Western blot results indicated that cordycepin could promote the expression of downstream antioxidant and anti-inflammatory factors and thereby reduce inflammation by activating Nrf-2 signaling pathway. Facts have proved that cordycepin has a protective effect on acute liver injury induced by CCl₄ in mice, and its mechanism is related to Nrf-2 signaling pathway.