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We further confirmed that HJT inhibits APAP-induced liver injury by blocking oxidative stress in vivo and identified indicators of the degree of liver damage in the serum and found that HJT reversed the increase in serum ALT/AST levels and cytokine release by APAP
This inhibits the ubiquitination and degradation of TAK1, increasing the stability and expression of TAK1 protein, activating the NF-B signaling pathway and NLRP3 inflammasome, promoting the release of inflammatory factors such as IL-1 and IL-18, and ultimately triggering pyroptosis in macrophages [144]
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It upregulates VEGF (vascular endothelial growth factor) and activates the VEGFR2 signaling pathway, creating new capillary networks that deliver oxygen and nutrients to injured tissue
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