Physical activity protects NLRP3 inflammasome-associated coronary vascular dysfunction in obese mice

• DOI: 10.14814/phy2.13738
• Publication Date: 2018-06-22T15:31:57Z
• Authors: Jonghae Lee; Yang Lee; Emily C. LaVoy; Michihisa Umetani; Junyoung Hong; Yoonjung Park
• Keywords: Endothelial Dysfunction; Pyrin domain

Activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome mediates release pro-inflammatory cytokine interleukin (IL)-1β and thereby plays a pivotal role in inflammatory response vascular pathology. An active lifestyle has beneficial effects on inflammation-associated dysfunction obesity. However, it remains unclear how physical activity regulates NLRP3 inflammasome-mediated Therefore, we explored protective effect inflammasome-associated mouse hearts, potential underlying mechanisms. C57BL/6J male mice were randomly divided into four groups: (1) control low-fat diet (LF-SED), (2) LF with free access to voluntary running wheel (LF-RUN), (3) high-fat (HF-SED; 45% calories from fat), (4) HF-RUN. We examined inflammasome-related signaling pathways, nitric oxide (NO) signaling, oxidative stress coronary arterioles test HFD activity. Voluntary reduced its downstream effects, caspase-1 IL-1β arteriole endothelium obese immunofluorescence staining. HF-RUN attenuated HFD-dependent endothelial NO synthase (eNOS) reduction thus increased production compared HF-SED. elevated intracellular superoxide while ameliorated stress. Our findings provide first evidence that attenuates activation feeding mice. Results further suggest improves obesity-induced by preserved bioavailability via restored expression eNOS