Methyl 3,4-dihydroxybenzoate protects against d-galN/LPS-induced acute liver injury by inhibiting inflammation and apoptosis in mice

Objectives Aimed to investigate the effect and mechanism of methyl 3,4-dihydroxybenzoate (MDHB) on d-galactosamine/lipopolysaccharide (d-galN/LPS)-induced acute liver failure (ALF). Methods Confirmed the hepatoprotective effect and hepatotoxicity of MDHB by histopathological examination (HE) and examination of alanine aminotransferase (ALT) and aspartate aminotransferase (AST); the expression of serum tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) was detected by ELISA; transcription levels of TNF-alpha, IL-1 beta, IL-6 and Toll-like receptor 4 (TLR4) were detected by qRT-PCR; and phosphorylation levels of p38 and p65 were analysed by Western blot. Results Histopathological examination and examination of ALT and AST confirmed that MDHB is a low toxicity drug that can resist d-galN/LPS-induced ALF; MDHB can effectively reduce high transcription and expression of TNF-alpha, IL-1 beta, IL-6 and TLR4 in d-galN/LPS-induced ALF; and Western blot showed that MDHB could down-regulate the expression of bax, up-regulate the expression of bcl-xl and bcl-2, and inhibit the phosphorylation of p38 and p65. Conclusions Methyl 3,4-dihydroxybenzoate can effectively resist d-galN/LPS-induced acute liver failure, which is related to the inhibition of inflammation and apoptosis.