Acute liver injury can be caused by chemicals and can lead to liver failure. We investigated the protective effect of helicid (HEL) on acute liver injury caused by CCl₄ in mice. We found that ALT and AST levels as well as hepatic pathological damage in mice treated with CCl₄ was increased significantly, while the effects were decreased by HEL treatment. HEL treatment increased the activity of T-SOD, GSH and CAT and reduced the level of MDA in CCl₄ treated mice. HEL improved the histopathology of liver caused by CCl₄. HEL also reduced TNF-α, IL-1β and IL- 6 activity caused by CCl₄. We investigated the phosphorylation of p65 and IκB protein and found that HEL can alleviate liver damage via the NF-κB signaling pathway. Our findings indicate that HEL protects against acute liver injury induced by CCl₄. The protective effect of HEL appears to be due to its antioxidative and anti-inflammatory properties through the NF-κB signaling pathway.

化学药品可导致急性肝损伤，并可导致肝衰竭。我们调查了Helicid（HEL）对CCl ₄引起的小鼠急性肝损伤的保护作用。我们发现，用CCl ₄处理的小鼠的ALT和AST水平以及肝病理损伤明显增加，而HEL处理则降低了影响。HEL处理可增加CCl ₄处理小鼠的T-SOD，GSH和CAT活性，并降低MDA含量。HEL改善了CCl ₄引起的肝脏组织病理学。HEL还降低了CCl ₄引起的TNF-α，IL-1β和IL-6活性。我们研究了p65和IκB蛋白的磷酸化，发现HEL可以通过NF-κB信号通路减轻肝脏损伤。我们的发现表明，HEL可预防CCl ₄引起的急性肝损伤。HEL的保护作用似乎归因于其通过NF-κB信号通路的抗氧化和抗炎特性。