Abstract
Free fatty acids (FFAs) are key players in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Inhibition of FFAs‐induced hepatic toxicity represents a potential therapeutic strategy. Glycyrrhizin (GL), the major bioactive component of licorice root extract, has been used to treat hepatitis to reduce liver inflammation and hepatic injury; however, the mechanism underlying the protective effect of GL remains unknown. GL exhibits its pharmacological functions through its biologically active metabolite, 18β glycyrrhetinic acid (GA), which is formed by presystemic hydrolysis. The aim of the present study was to examine if GA is able to prevent FFAs‐induced lipotoxicity and identify the potential cellular mechanisms. Both in vitro FFAs‐induced HepG2 NAFLD model and in vivo high fat diet (HFD)‐induced rat NAFLD model were used in the current studies.Results: GA not only prevented FFAs‐induced lipoapoptosis in HepG2 cells, but also prevented HFD‐induced liver injury in in vivo rat models. Furthermore, stabilization of lysosomal membrane, inhibition of cathepsin B expression and enzyme activity, inhibition of mitochondrial cytochrome c release, and reduction of oxidative stress represent the major cellular mechanisms underlying its protective effects on FFAs/HFD‐induced hepatic lipotoxicity.Conclusion: GA may be beneficial for preventing FFAs/HFD‐induced lipotoxicity or treating NAFLD.
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