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水通道蛋白在肥胖中的作用 被引量:1
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作者 gema fruhbeck 林益华 《中国糖尿病杂志》 CAS CSCD 北大核心 2006年第5期400-400,共1页
关键词 水通道蛋白 肥胖 家族成员 脂肪代谢 膜通道 水平衡 节细胞 蛋白原
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NLRP3 inflammasome blockade reduces adipose tissue inflammation and extracellular matrix remodeling 被引量:15
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作者 Xabier Unamuno Javier Gomez-Ambrosi +8 位作者 Beatriz Ramirez Amaia Rodriguez Sara Becerril Victor Valenti Rafael Moncada Camilo Silva Javier Salvador gema fruhbeck Victoria Catalan 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2021年第4期1045-1057,共13页
The NLRP3-IL-1β pathway plays an important role in adipose tissue(AT)-induced inflammation and the development of obesityassociated comorbidities.We aimed to determine the impact of NLRP3 on obesity and its associate... The NLRP3-IL-1β pathway plays an important role in adipose tissue(AT)-induced inflammation and the development of obesityassociated comorbidities.We aimed to determine the impact of NLRP3 on obesity and its associated metabolic alterations as well as its role in adipocyte inflammation and extracellular matrix(ECM)remodeling.Samples obtained from 98 subjects were used in a case-control study.The expression of different components of the inflammasome as well as their main effectors and inflammation-and ECM remodeling-related genes were analyzed.The impact of blocking NLRP3 using siRNA in lipopolysaccharide(LPS)-mediated inflammation and ECM remodeling signaling pathways was evaluated.We demonstrated that obesity(P<0.01),obesity-associated T2D(P<0.01)and NAFLD(P<0.05)increased the expression of different com ponents of the inflammasome as well as the expression and release of IL-1β and IL-18 in AT.We also found that obese patients with T2D exhibited increased(P<0.05)hepatic gene expression levels of NLRP3,IL1B and IL18.We showed that NLRP3,but not NLRP1,is regulated by inflammation and hypoxia in visceral adipocytes.We revealed that the inhibition of NLRP3 in human visceral adipocytes significantly blocked(P<0.01)LPS-induced inflammation by downregulating the mRNA levels of CCL2,IL1B,IL6,IL8,S100A8,S100A9,TLR4 and TNF as well as inhibiting(P<0.01)the secretion of IL1-β into the culture medium.Furthermore,blocking NLRP3 attenuated(P<0.01)the LPS-induced expression of important molecules involved in AT fibrosis(COL1A1,COL4A3,COL6A3 and MMP2).These novel findings provide evidence that blocking the expression of NLRP3 reduces AT inflammation with significant fibrosis attenuation. 展开更多
关键词 NLRP3 Inflammasone INFLAMMATION OBESITY Type 2 diabetes Nonalcoholic fatty liver disease
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