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.