Beneficial Effects of lncRNA-UC.360+shRNA on Diabetic Cardiac Sympathetic Damage via NLRP3 Inflammasome-Induced Pyroptosis in Stellate Ganglion

Hyperglycemia is one of the common symptoms of diabetes, and it produces excessive reactive oxygen species (ROS). This study investigated whether the long noncoding RNA (lncRNA) UC.360+ is involved in diabetic cardiac autonomic neuropathy (DCAN) mediated by NLRP3 inflammasome-induced pyroptosis in the stellate ganglion (SG). Using a rat type 2 diabetes model, we found that lncRNA UC.360+ short hairpin RNA (shRNA) ameliorated the dyslipidaemia of type 2 diabetic rats and reduced serum adrenaline and ROS production in SG under hyperglycemia. In addition, UC.360+ shRNA also reduced the expression of nuclear factor kappa-B (NF -KB), NLRP3, ASC, caspase-1, interleukin-1 beta (IL-1 beta), and IL-18 in the SG of diabetic rats and inhibited the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK). Therefore, lncRNA-UC.360+ shRNA may modulate the NLRP3 inflammasome/inflammatory pathway in the SG, which in turn alleviates diabetic heart sympathetic nerve damage.

Automated summary

This study found that lncRNA-UC.360+ shRNA can alleviate dyslipidemia in type 2 diabetic rats, reduce serum adrenaline and ROS production in the stellate ganglion under hyperglycemia conditions. Additionally, UC.360+ shRNA also modulates the inflammatory pathway by reducing the expression of NF-KB, NLRP3, ASC, caspase-1, IL-1β, IL-18, and inhibiting the phosphorylation of p38 MAPK, thus alleviating diabetic heart sympathetic nerve damage.