1. MPST attenuates H2S production and subsequently promotes fat accumulation in hepatocytes through CSE dependent-mechanism.
MPST attenuates H2S production and subsequently promotes fat accumulation in hepatocytes through CSE dependent-mechanism. (A–C) After transfection with scrambled siRNA (negative control) and MPST siRNA for 24 hours, L02 cells were transfected with or without CSE siRNA for 24 hours. Then the cells were treated with FFAs (1 mM) for another 24 hours and subjected to western blot analyses (A). The fresh supernatants were collected to measure H2S levels (B). Representative Oil Red O staining images and measurements of intracellular TG content are shown in (C). Original magnification ×400. (D) The correlation between supernatant H2S levels and intracellular TG contents in FFA-treated L02 cells was analysed. (E) L02 cells transfected with MPST siRNA and CSE siRNA were pretreated with NaHS (1 mM) for 2 hours and then treated with FFAs (1 mM) with or without NaHS for 24 hours. Intracellular TG contents were determined. (F) L02 cells were pretreated with NaHS (1 mM) for 2 hours and then treated with FFAs (1 mM) with or without NaHS for 24 hours. Representative Oil Red O staining images and measurements of intracellular TG contents were shown. The results are expressed as the mean±SD of three independent experiments. *p<0.05, **p<0.01, ***p< CSE, cystathionine γ-lyase; FFA, free fatty acid; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; H2S, hydrogen sulfide; MPST, 3-mercaptopyruvate sulfurtransferase; NaHS, sodium hydrosulfide; siRNA, small interfering RNA; TG, triglyceride.
Meng Li et al. Gut 2018;67:
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