Asprosin promotes vascular inflammation via TLR4-NFκB-mediated NLRP3 inflammasome activation in hypertension.

Objective: and design Mild vascular inflammation promotes the pathogenesis of hypertension. Asprosin, a newly discovered adipokine, is closely associated with metabolic diseases. We hypothesized that asprosin might led to vascular inflammation in hypertension via NLRP3 inflammasome formation. This study shows the importance of asprosin in the vascular inflammation of hypertension. Methods: Primary vascular smooth muscle cells (VSMCs) were obtained from the aorta of animals, including spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), NLRP3-/- and wild-type mice. Studies were performed in VSMCs in vitro, as well as WKY and SHR in vivo. Results: Asprosin expressions were up-regulated in VSMCs and media of arteries in SHR. Asprosin overexpression promoted NLRP3 inflammasome activation via Toll-like receptor 4 (TLR4), accompanied with activation of NFκB signaling pathway in VSMCs. Exogenous asprosin protein showed similar roles in promoting NLRP3 inflammasome activation. Knockdown of asprosin restrained NLRP3 inflammasome and p65-NFκB activation in VSMCs of SHR. NLRP3 inhibitor MCC950 or NFκB inhibitor BAY11-7082 attenuated asprosin-caused VSMC proliferation and migration. Asprosin-induced interleukin-1ß production, proliferation and migration were attenuated in NLRP3-/- VSMCs. Local asprosin knockdown in common carotid artery of SHR attenuated inflammation and vascular remodeling. Conclusions: Asprosin promoted NLRP3 inflammasome activation in VSMCs by TLR4-NFκB pathway, and thereby stimulates VSMCs proliferation, migration, and vascular remodeling of SHR.

Lethal activity of nonthermal plasma sterilization against microorganisms.

OBJECTIVE: To determine the range and the mode of germicidal activity of sterilants generated by a nonthermal plasma sterilization system for microorganisms. METHODS: Representative bacteria, spores, viruses, bacteriophages, and fungi were exposed to the plasma cycle and the residual viability was measured in vitro. To assess the mode of lethal injury, Escherichia coli, Staphylococcus aureus, Bacillus atrophaeus, and bacteriophages were exposed to the plasma cycle, and the effects of the plasma-generated sterilants on the biological parameters were determined. RESULTS: There were at least 4-6 log reductions in viability for all microorganisms after 10 minutes of exposure to the plasma cycle. Electron micrographs and studies of the inhibition of bacteriophage infectivity suggested that the primary injury is to the organisms' cell envelopes. The plasma cycle also denatured isolated bacterial proteins and inactivated bacteriophages, but it had no effect on isolated DNA and bacterial proteins within exposed bacteria. CONCLUSION: Nonthermal plasma, which is produced at atmospheric temperature and pressure, generates sterilants that kill high concentrations of microorganisms and inactivate viruses during a 10-minute exposure. The primary injury appears to be at the surface structures of the organisms. This suggests that nonthermal plasma has utility for sterilization of heat-sensitive medical materials and devices.