AbstractFatty acids induced hepatic inflammation plays an important role in
nonalcoholic fatty liver disease (NAFLD) pathogenesis. Hydrogen sulfide
(H2S), an endogenous gasotransmitter, has been established to
possess potent anti-inflammation in various human organs. However, the
anti-inflammation property of H2S in the fatty liver is still
needed to further elucidate. Hence, this study aimed to investigate whether
exogenous H2S can protect hepatocytes against inflammation
induced by palmitic acid (PA). HepG2 hepatocytes were exposed to PA for
24 h to induce free fatty acids-induced inflammation. The cells were
pretreated with NaHS (a donor of H2S) before exposure to PA. Cell viability,
inflammatory cytokines (TNF-α, IL-6 and IL-1β), NLRP3
inflammasome and NF-κB were measured by a combination of MTT assay,
ELISA, Western blot and Immunofluorescence. Here, we found that exogenous
H2S dose-dependently inhibited the expression of
pro-inflammatory cytokines, NLRP3 inflammasome and activation of
NF-κB signaling in PA-induced HepG2 cells. Thus, H2S
might be a candidate therapeutic agent against NAFLD.
Hydrogen sulfide and nonalcoholic fatty liver disease
