Human NLRP3(Nod Like Receptor Pyrins-3) ELISA Kit

Autophagy and NLRP3 inflammasome were associated with the process of colitis. Drugs targeting NLRP3 inflammasome and autophagy to treat colitis are absent, and they are urgently required. Herein, we examine the effect of evodiamine, extracted from the fruit of Evodiae Fructus, on experimental colitis induced by dextran sulfate sodium and exposit whether evodiamine effects on autophagy and NLRP3 inflammasome. Our data indicated that colitis was ameliorated by evodiamine, including the improvement of mice body weight, colon length, histopathologic score, and the disease activity index. We also observed that evodiamine restrained the formation of the NLRP3 inflammasome by inhibiting the apoptosis-associated speck-like protein oligomerization and caspase-1 activity in THP-1 macrophages. Our results demonstrated evodiamine inhibit NLRP3 inflammasome activation via the induction of autophagosome-mediated degradation of inflammasome and the inhibition of NF kappa B pathway, which synergistically contribute to the effect of evodiamine in colitis. It indicates the potential use of evodiamine in inflammatory bowel diseases treatment.

Aims/Introduction Micro-ribonucleic acids (miRNAs) possess crucial functions in governing metabolisms associated with type 2 diabetes mellitus. This study aimed to investigate the role of miR-23a-3p in pyroptosis caused by nucleotide-binding oligomerization-like receptor family pyrin domain containing 3 (NLRP3) inflammatory body activation, thereby reducing the occurrence of type 2 diabetes mellitus. Materials and Methods miR-23a-3p and NIMA-related kinase 7 (NEK7) expression in type 2 diabetes mellitus patients and rat models was examined. Dual-luciferase reporter gene experiments were used to verify the targeting relationship between miR-23a-3p and NEK7. Bone marrow-derived macrophages were transfected with miR-23a-3p mimic, miR-23a-3p inhibitor or short hairpin NEK7 and were treated with a specific activator of NLRP3 inflammatory body (lipopolysaccharide + adenosine-5 '-triphosphate) to evaluate expression of NEK7, miR-23a-3p, gasdermin D p30, pro-caspase-1 and caspase-1 in cells, and interleukin-1 beta and tumor necrosis factor-alpha in supernatant. Type 2 diabetes mellitus rat models were used to observe the influences of miR-23a-3p, NEK7 and NLRP3 inflammatory body on pyroptosis and type 2 diabetes mellitus in vivo. Results NEK7 was overexpressed, whereas miR-23a-3p was underexpressed in patients and rat models with type 2 diabetes mellitus. NEK7 was a target gene of miR-23a-3p. After the addition of lipopolysaccharide + adenosine-5 '-triphosphate in bone marrow-derived macrophages, the expression of miR-23a-3p subsequently declined. Furthermore, the addition of lipopolysaccharide + adenosine-5 '-triphosphate elevated NEK7, NLRP3, pro-caspase-1, cle-caspase-1 and gasdermin D p30 expressions in bone marrow-derived macrophages, and enhanced levels of interleukin-1 beta and tumor necrosis factor-alpha in the supernatant, accompanied with conspicuous cell pyroptosis, which was reversed after miR-23a-3p overexpression and NEK7 silencing. miR-23a-3p overexpression alleviated liver and kidney damage in type 2 diabetes mellitus rats, and reduced NLRP3-induced pyroptosis. Conclusions Targeting NEK7 by miR-23a-3p could reduce NLRP3-induced pyroptosis, and assuage liver and kidney injuries in type 2 diabetes mellitus rats.