Astragaloside IV combating liver cirrhosis through the PI3K/Akt/mTOR signaling pathway

Astragaloside IV (AS-IV) in improving liver cirrhosis injury in rats and its effect on the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway were observed. Rat model of liver cirrhosis was induced by injection of carbon tetrachloride (CCl4). A total of 36 Sprague-Dawley (SD) rats were randomly divided into three groups: the normal control group (n=10), the model control group (n=13), and the AS-IV group (n=13). The normal control group was injected with olive oil and given carboxymethyl cellulose (CMC)-Na (10 ml/kg/day), the model control group was given CMC-Na (10 ml/kg/day), and the AS-IV group underwent intragastric administration of AS-IV (20 ml/kg/day). The content of alanine transaminase (ALT) and aspartate transaminase (AST) of rats was detected. The levels of tumor necrosis factor- (TNF-), interleukin (IL)-6 and IL-1 in serum were detected via enzyme-linked immunosorbent assay (ELISA). Hematoxylin and eosin (H&E) staining was applied to observe morphological changes in liver tissues. The expression of collagens in liver tissues was detected via Masson's trichrome staining. Additionally, the expression of proteins in liver tissues was detected via western blotting. Compared with those in the blank group, the levels of AST, ALT, TNF-, IL-6 and IL-1 were higher, the expression level of collagens in liver tissues was increased, and the expression ratios of phosphorylated (p)-PI3K/PI3K, p-Akt/Akt and p-mTOR/mTOR proteins were increased in the model group. Compared with the model group, AS-IV could significantly decrease the content of AST, ALT, TNF-, IL-6 and IL- in serum of rats, obviously inhibit the expression of collagens in liver tissues and decrease the expression ratios of p-PI3K/PI3K, p-Akt/Akt and p-mTOR/mTOR proteins in liver tissues. AS-IV can inhibit the inflammatory response so as to reduce the expression of collagens, and its mechanism may play a key role by inhibiting the PI3K/Akt/mTOR signaling pathway.