scholarly journals AdipoRon Alleviates Free Fatty Acid-Induced Myocardial Cell Injury Via Suppressing Nlrp3 Inflammasome Activation

2019 ◽  
Vol Volume 12 ◽  
pp. 2165-2179 ◽  
Author(s):  
You-Zhi Zhang ◽  
Yu-Lin Zhang ◽  
Qi Huang ◽  
Cong Huang ◽  
Zhi-Long Jiang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Nlrp3 Inflammasome ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Myocardial Cell Injury

scholarly journals Protection of Sacubitril/Valsartan against Pathological Cardiac Remodeling by Inhibiting the NLRP3 Inflammasome after Relief of Pressure Overload in Mice

2020 ◽  
Vol 34 (5) ◽  
pp. 629-640
Author(s):  
Xueling Li ◽  
Qin Zhu ◽  
Qingcheng Wang ◽  
Qinggang Zhang ◽  
Yaru Zheng ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Cardiac Remodeling ◽  
Cardiac Fibrosis ◽  
Pressure Overload ◽  
Myocardial Cell ◽  
Heart Weight ◽  
Inflammasome Activation ◽  
Clinical Prognosis ◽  
Nlrp3 Inflammasome Activation ◽  
Neprilysin Inhibitor

Abstract Background/aims The persistent existence of pathological cardiac remodeling, resulting from aortic stenosis, is related to poor clinical prognosis after successful transcatheter aortic valve replacement (TAVR). Sacubitril/valsartan (Sac/Val), comprising an angiotensin receptor blocker and a neprilysin inhibitor, has been demonstrated to have a beneficial effect against pathological cardiac remodeling, including cardiac fibrosis and inflammation in heart failure. The aim of this study was to determine whether Sac/Val exerts a cardioprotective effect after pressure unloading in mice. Methods and results Male C57BL/6 J mice were subjected to debanding (DB) surgery after 8 weeks (wk) of aortic banding (AB). Cardiac function was assessed by echocardiography, which indicated a protective effect of Sac/Val after DB. After treatment with Sac/Val post DB, decreased heart weight and myocardial cell size were observed in mouse hearts. In addition, histological analysis, immunofluorescence, and western blot results showed that Sac/Val attenuated cardiac fibrosis and inflammation after DB. Finally, our data indicated that Sac/Val treatment could significantly suppress NF-κB signaling and NLRP3 inflammasome activation in mice after relief of pressure overload. Conclusion Sac/Val exerted its beneficial effects to prevent maladaptive cardiac fibrosis and dysfunction in mice following pressure unloading, which was at least partly due to the inhibition of NLRP3 inflammasome activation.

scholarly journals UCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis

2015 ◽  
Vol 125 (2) ◽  
pp. 665-680 ◽  
Author(s):  
Jong-Seok Moon ◽  
Seonmin Lee ◽  
Mi-Ae Park ◽  
Ilias I. Siempos ◽  
Maria Haslip ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nlrp3 Inflammasome ◽  
Fatty Acid Synthase ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

scholarly journals PF-04620110, a Potent Antidiabetic Agent, Suppresses Fatty Acid-Induced NLRP3 Inflammasome Activation in Macrophages

2019 ◽  
Vol 43 (5) ◽  
pp. 683
Author(s):  
Seung Il Jo ◽  
Jung Hwan Bae ◽  
Seong Jin Kim ◽  
Jong Min Lee ◽  
Ji Hun Jeong ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Antidiabetic Agent ◽  
Nlrp3 Inflammasome Activation

scholarly journals Triptolide Inhibits the Activation of NLRP3 Inflammasome by Inhibiting NF-κB Pathway and Improves Myocardial Fibrosis

2021 ◽  
Author(s):  
Jianyao Shen ◽  
Hailiang Ma ◽  
Chaoquan Wang
Keyword(s):  
Myocardial Fibrosis ◽  
Nlrp3 Inflammasome ◽  
Subcutaneous Injection ◽  
Tissue Injury ◽  
Myocardial Cell ◽  
Inflammatory Factors ◽  
Inflammasome Activation ◽  
Related Factors ◽  
Nlrp3 Inflammasome Activation ◽  
Tnf Α

Abstract ObjectiveTriptolide (TPL) is identified to be involved in the treatment for myocardial fibrosis (MF). This study investigated the mechanism of TPL in MF in rats and observed its effect on NLRP3 inflammasome signaling pathway.Materials and MethodsThe MF rat model was established by subcutaneous injection of isoproterenol (ISO), and treated by subcutaneous injection of TPL. After modeling for 1 week, the cardiac function of rats was evaluated, including LVEF, LVFS, LVES, LVED LVIDs and LVPWs. The HMI and LVMI were measured. The expressions of ANP, BNP, inflammatory related factors (IL-1β, IL-18, TNF-α, MCP-1, VCAM-1), and NLRP3 inflammasome factors (NLRP3, ASC, caspase-1) in rats were detected. HE staining and Masson staining were used to observe myocardial cell inflammation and fibrosis of rats.ResultsLVED, LVES, LVIDs and LVPWs of MF group were significantly upregulated, LVEF and LVFS were significantly downregulated, HMI and LVMI were upregulated, while TPL treatment reversed these trends; TPL treatment downregulated the tissue injury and improved the pathological damage of MF rats. TPL treatment downregulated the levels of inflammatory factors and fibrosis factors, and inhibited the activation of NLRP3 inflammasome. Activation of NLRP3 inflammasome or NF-κB pathway reversed the effect of TPL on MF.ConclusionsTPL inhibited the activation of NLRP3 inflammasome by inhibiting NF-κB pathway, and improved the degree of MF in MF rats.

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