NALM improves CCl4-induced liver injury and may be a potential treatment option for PeALT in patients with CHB
To explore the potential role of differential metabolites in ALT elevation, we established a mouse model of liver injury by inducing liver damage using CCl4 to simulate the ALT elevation observed in patients with CHB (Figure 4A). After 24 h of CCl4 stimulation, the serum ALT levels of mice significantly increased, peaking at 48 h, and then decreasing significantly at 72 h, indicating regression in liver injury. Notably, we found that at 48 and 72 h after CCl4 stimulation, ALT levels in the CCl4+NALM (i.p.) group were significantly lower than those in the CCl4+PBS (i.p.) group, indicating that NALM supplementation alleviated the liver injury induced by CCl4 (Figure 4B). In addition, ALT levels in the CCl4+3-Mx (i.g.) group were significantly reduced compared to those in the CCl4+PBS (i.g.) group at 48 h. At 72 h, the ALT levels in the CCL4+3-MA (i.g.) group were significantly higher than those in the CCl4+PBS (i.g.) group, indicating that 3-MA may hinder the regression of liver injury (Figure 4C). Subsequently, we evaluated the roles of these metabolites on AST levels. NALM, 7-Mx and 3-Mx significantly inhibited the increase in AST caused by CCL4 (Figure 4D and 4E). Further pathological analysis suggested that NALM supplementation significantly reduced CCl4-induced necrosis compared to that in the CCl4+PBS (i.p.) group (Figure 4F and 4G). Overall, NALM may improve liver injury, promote the recovery of liver function, and be a potential treatment for PeALT in patients with CHB.