Objective: To study the protective effect and mechanism of methyl helicterate isolated from Helicteres Radix on chronic liver injury induced by carbon tetrachloride (CCl4) in rats. Method: The rats were randomly divided into 5 groups

including normal control group

model group

silymarin positive control group(50 mg·kg-1)

and high and low-dose methyl helicterate (200

50 mg·kg-1) groups. Except for the normal control group

all of the other groups were intragastrically administrated with 20% CCl4 for 8 weeks

twice a week. Meanwhile

the animals in the positive control group and methyl helicterate-treated groups were given silymarin (50 mg·kg-1) and methyl helicterate (200

50 mg·kg-1) by gavage once a day for 8 weeks. After the experiment

the levels of serum alanine aminotransferase (ALT)

aspartate aminotransferase (AST)

albumin (ALB) and plasma interleukin-6 (IL-6)

tumor necrosis factor -α (TNF-α) were detected by enzyme-linked immuno sorbent assay(ELISA) kits. The hepatic pathological changes were observed by HE staining. And the levels of superoxide dismutase (SOD)

glutathione peroxidase (GSH-Px)

glutathione reductase (GSH-Rd)

NF-κB p65 in liver tissues were detected by ELISA kits. Western blot assay was performed to detect the expression of nitric oxide synthase (iNOS)

cyclooxygenase-2 (COX-2)

Caspase-3

Caspase-8 Fas and FasL in liver tissues. Result: Methyl helicterate significantly alliviated CCl4-induced serious liver injury

decreased the levels of serum ALT

AST and ALB

while increased the activities of hepatic SOD

GSH-Px and GSH-Rd. Methyl helicterate also reduced the contents of inflammatory cytokines TNF-α and IL-6 in liver tissues. The further study showed that methyl helicterate significantly inhibited the vitality of NF-κB

iNOS and COX-2

which played a crucial role in regulat inginflammatory response.In addition

methyl helicterate significantly suppressed the expressions of Caspase-3

Caspase-8

Fas and FasL

and reduced the hepatocytes apoptosis. Conclusion: Methyl helicterate alleviates liver injury induced by CCl4 in rats

the mechanism may be associated with the inhibition of NF-κB signaling pathway and the decrease in cell apoptosis.