P2668Liraglutide attenuates NLRP3 inflammasome-dependent pyroptosis via regulating SIRT1/NOX4/ROS pathway in H9c2 cells

Chen, A; Chen, Z W; Yan, Xia; Lu, Danbo; Yang, Xinrong; Sun, Aijun; Zou, Ying; Qian, Jing; Ge, Junbo

doi:10.1093/eurheartj/ehy565.p2668

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“…Pyroptosis is a form of procedural cell death that causes rapid cell lysis [50] and is associated with a variety of physiological and pathological conditions, including oxidative stress damage caused by ROS overdose [51], which may lead to flap necrosis. Liraglutide has been reported to improve nonalcoholic fatty hepatitis and protect myocardial cells by inhibiting NLRP3 inflammasome-dependent pyroptosis [28,52]. The NLRP3 inflammasome is a multiprotein platform that is activated when cells are infected or stressed, leading to the secretion of caspase-1-dependent proinflammatory cytokines (such as IL-1β and IL-18) that trigger pyroptosis [53,54].…”

Section: Discussionmentioning

confidence: 99%

Liraglutide, a TFEB‐Mediated Autophagy Agonist, Promotes the Viability of Random‐Pattern Skin Flaps

Zhu

Lou

et al. 2021

Oxidative Medicine and Cellular Longevity

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Random skin flaps are commonly used in reconstruction surgery. However, distal necrosis of the skin flap remains a difficult problem in plastic surgery. Many studies have shown that activation of autophagy is an important means of maintaining cell homeostasis and can improve the survival rate of flaps. In the current study, we investigated whether liraglutide can promote the survival of random flaps by stimulating autophagy. Our results show that liraglutide can significantly improve flap viability, increase blood flow, and reduce tissue oedema. In addition, we demonstrated that liraglutide can stimulate angiogenesis and reduce pyroptosis and oxidative stress. Through immunohistochemistry analysis and Western blotting, we verified that liraglutide can enhance autophagy, while the 3-methylladenine- (3MA-) mediated inhibition of autophagy enhancement can significantly reduce the benefits of liraglutide described above. Mechanistically, we showed that the ability of liraglutide to enhance autophagy is mediated by the activation of transcription factor EB (TFEB) and its subsequent entry into the nucleus to activate autophagy genes, a phenomenon that may result from AMPK-MCOLN1-calcineurin signalling pathway activation. Taken together, our results show that liraglutide is an effective drug that can significantly improve the survival rate of random flaps by enhancing autophagy, inhibiting oxidative stress in tissues, reducing pyroptosis, and promoting angiogenesis, which may be due to the activation of TFEB via the AMPK-MCOLN1-calcineurin signalling pathway.

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