Treatment of Hippophae rhamnoides Polysaccharides on Alcoholic Hepatitis and Intestinal Barrier Function in Mice

Objective: To investigate the protective effects of sea buckthorn polysaccharides (Hippophae rhamnoides Polysaccharides, HRP) on alcoholic hepatitis (AH) and its underlying mechanisms, particularly its effect on the impairment of hepatitis and intestinal barrier in mice. Methods: A mouse model of alcoholic hepatitis was established, and the mice were administered with sea buckthorn polysaccharides (low dose of 100 mg/kg and high dose of 200 mg/kg) by gavage once daily. Effects of HRP on plasma biochemical parameters, liver tissue biochemical indicators, and pathological morphological changes in liver and intestinal tissues were observed. Additionally, the effect of HRP on intestinal permeability, inflammation in colon tissue, and intestinal barrier function was analyzed. Results: Compared with the model group, the levels of AST and ALT in plasma significantly decreased, while ALB increased significantly in the low and high dose HRP groups (P<0.01 or P<0.05). HRP at both low and high doses significantly reduced the levels of TC, TG, LDL-C, and FFA in plasma and increased the level of HDL-C (P<0.01 or P<0.05). In the liver tissue, HRP significantly reduced the contents of TG and TC, decreased the levels of pro-inflammatory factors IL-6, IL-1β, and TNF-α, and increased the levels of liver SOD and GSH, while reducing MDA levels (P<0.01 or P<0.05). Histopathological examination revealed that HRP improved liver structure, reduced fatty degeneration, and inflammatory cell infiltration. Furthermore, HRP significantly reduced plasma LPS and D-lactic acid levels, improved intestinal histopathological changes, increased the expression level of tight junction proteins, and decreased the expression of colonic inflammatory factors (P<0.01 or P<0.05). Conclusion: HRP has a protective effect on alcoholic hepatitis, improving liver damage and intestinal barrier function in mice, and reducing liver lipid accumulation and inflammatory response.