Ginsenoside Rb2 improves insulin resistance by inhibiting adipocyte pyroptosis

ABSTRACT

Pyroptosis plays a critical role in the development of obesity-associated inflammation and insulin resistantance (IR). Ginsenoside Rb2 (Rb2), the main component of ginsenosides has drawn appreciable interest in the context of glucose metabolism. In the present study, we investigated Rb2-mediated protection against obesity-induced IR and the related mechanisms. Rb2 could significantly reduce high-fat diet (HFD)-induced body weight changes, fat accumulation and IR. In addition, Rb2 treatment inhibited pyroptosis-related genes and proteins, such as caspase-1, ASC, NLRP3, IL-1β and GSDMD in HFD-fed mice. The above results were recapitulated in 3T3-L1 adipocytes and demonstrated that Rb2 improved TNF-α induced IR and pyroptosis in 3T3-L1 adipocytes. Furthermore, Rb2 reduced the phosphorylation levels of p65 and IκBα both in vitro and in vivo. The present study showed that Rb2, which could serve as a promising agent for the treatment of IR and obesity, ameliorated IR by inhibiting pyroptosis in adipocytes in vivo and in vitro through the NF-κB pathway.

KEYWORDS:

• Ginsenoside Rb2
• insulin resistant
• pyroptosis
• NLRP3 inflammasome
• NF-Κb signalling pathway

Disclosure statement

No potential conflict of interest was reported by the authors.

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Funding

This work was supported by grant from Zhejiang Provincial Natural Science Foundation under Grant [LY20H070003 and LQ12H07003], the Wenzhou Science & Technology Bureau under Grant [Y20170047] and the National Key R&D Program of China under Grant [2016YFC1305202].