Exploring the mechanisms of Yinlai Decoction intervening the mice model of FM1 virus infected compound with high-fat and protein-diet

Abstract

ObjectiveTo explore the mechanism of Yinlai Decoction (YD) intervening the mice model of FM1 influenza virus compound with high-fat and protein-diet by detecting the survival rate, lung injury, the expression of inflammatory cytokines. MethodsA high-fat and protein-diet mouse model was built. Mice were randomly divided to groups of blank control, normal diet, high-fat and protein-diet (HPD), the Ribavirin, the Shuanghuanglian, the Xiaoer huashi Pill and the YD, all infected with FM1 virus via nose after four days' high-fat and protein-diet. The electrogastrography (EGG) was recorded, as well as the serum levels of the gastrin and plasma vasoactive intestinal peptide (VIP) were observed. Mice in the blank control group were shame-infected with 0.05 mL saline, while the mice in other groups were infected by 0.05 mL mouse lung-adapted FM1 virus. Interventions were performed by stomach perfusion for next seven days. Same dose saline was given in the blank control, normal diet and HPD groups. The life protection and mean survival days were calculated. The lung injuries were observed by H&E method. The expression of gastrin and VIP were detected by radioimmunoassay. The serum levels of IFN-γ, IL-4, IL-6, IL-10 and TNF-α were measured by ELISA. ResultsCompared with normal diet group, EGG dominant frequency, EGG swing, instability coefficient increased in HPD group. Compared with HPD group, Ribavirin group and YD group showed significantly higher survival rate and IL-10 and IFN-γ levels significantly increased while the IL-6 and TNF-α levels significantly decreased. Compared with blank control group, severe lung cirrhosis injuries were found in HPD group, and mild injuries were found in YD group and Ribavirin group. ConclusionsThe YD can regulate the level of cytokines, and improve the pathological damages of lung tissue, and then protect the mice with high-fat and protein-diet from being injured from the FM1 virus.