Abstract： Objective： To investigate the effects and mechanisms of Sijunzi Decoction combined with Sanzi Yangqin Decoction（SJZ+SZ）on early and advanced stages of metabolic dysfunction-associated steatotic liver disease （MASLD）in mice，based on the method of fortifying the spleen and dissolving phlegm. Methods：The Gubra-Amylin NASH（GAN）diet was used to induce MASL in C57BL/6J mice. Mice were then treated with SJZ，SZ，or SJZ+SZ via gavage for four weeks. Additionally，metabolic dysfunction-associated steatohepatitis（MASH）was induced in C57BL/ 6J mice using a high-fat diet and high-fructose/glucose drinking water. These mice were treated with SZ or SJZ+SZ via gavage for eight weeks（since SJZ showed no significant effect in the MASL model，no SJZ group was set for the MASH model）. Mouse body weight and liver weight were recorded；liver tissue pathology was observed；hepatic lipid levels and serum transaminases，as well as tumor necrosis factor-α（TNF-α）levels，were measured. Western Blot was used to detect the expression levels of inflammation and fibrosis-related molecules in liver tissue. The insulin resistance index （HOMA-IR）was calculated for each group of mice， and the expression levels of IRS1 / Akt activation and lipid synthesis-related molecules in liver tissue were detected using Western Blot and RT-qPCR. Results：In the MASL mouse model，both SJZ+SZ and SZ reduced the degree of hepatic steatosis，decreased hepatic triglyceride（TG）levels and serum transaminase levels in model mice（P＜0.05），while SJZ showed no significant improvement in MASL（P＞ 0.05）. In the MASH model mice experiment，SJZ or SZ significantly reduced body weight，liver weight，and liver tissue pathological damage in MASH mice（P＜0.05），decreased hepatic TG content and serum transaminase and TNF- α levels（P＜0.05）， and reversed the expression levels of inflammatory factors（interleukin-1β， TNF - α， and interleukin-10）and fibrosis-related molecules（transforming growth factor-β 1 ，α-smooth muscle actin，and type Ⅰ collagen α1）in liver tissue（P＜0.05）；the SZ had no significant effect on these indicators in MASH mice（P＞0.05）. Additionally， SJZ + SZ significantly downregulated the elevated blood glucose， insulin levels， and HOMA-IR in MASH mice（P＜0.05），reversed the downregulated levels of insulin receptor substrate 1，threonine protein kinase， and acetyl-CoA carboxylase phosphorylation in liver tissue of model mice（P＜0.05），and inhibited the expression of lipid synthesis-related molecules，including sterol regulatory element-binding protein1c，and fatty acid synthase（P＜ 0.05）；SZ only showed a downward trend in these indicators（P＞0.05）. Conclusion：The SJZ had no significant effect on MASLD in mice. SZ only improved MASLD to a certain extent in the less severe cases. The SJZ+SZ improved MASLD in mice at different stages，with insulin resistance regulation being part of its mechanism of action.