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α1-AR overactivation induces cardiac inflammation through NLRP3 inflammasome activation

  
@article{APS10101,
	author = {Jun-zhou Xin and Ji-min Wu and Guo-min Hu and Hui-jun Gu and Ye-nan Feng and Shuai-xing Wang and Wen-wen Cong and Ming-zhe Li and Wen-li Xu and Yao Song and Han Xiao and You-yi Zhang and Li Wang},
	title = {α 1 -AR overactivation induces cardiac inflammation through NLRP3 inflammasome activation},
	journal = {Acta Pharmacologica Sinica},
	volume = {41},
	number = {3},
	year = {2020},
	keywords = {},
	abstract = {Acute sympathetic stress causes excessive secretion of catecholamines and induces cardiac injuries, which are mainly mediated by β-adrenergic receptors (β-ARs). However, α1-adrenergic receptors (α1-ARs) are also expressed in the heart and are activated upon acute sympathetic stress. In the present study, we investigated whether α1-AR activation induced cardiac inflammation and the underlying mechanisms. Male C57BL/6 mice were injected with a single dose of α1-AR agonist phenylephrine (PE, 5 or 10 mg/kg, s.c.) with or without pretreatment with α-AR antagonist prazosin (5 mg/kg, s.c.). PE injection caused cardiac dysfunction and cardiac inflammation, evidenced by the increased expression of inflammatory cytokine IL-6 and chemokines MCP-1 and MCP-5, as well as macrophage infiltration in myocardium. These effects were blocked by prazosin pretreatment. Furthermore, PE injection significantly increased the expression of NOD-like receptor protein 3 (NLRP3) and the cleavage of caspase-1 (p20) and interleukin-18 in the heart; similar results were observed in both Langendorff-perfused hearts and cultured cardiomyocytes following the treatment with PE (10 μM). Moreover, PE-induced NLRP3 inflammasome activation and cardiac inflammation was blocked in Nlrp3-/- mice compared with wild-type mice. In conclusion, α1-AR overactivation induces cardiac inflammation by activating NLRP3 inflammasomes.},
	url = {http://www.chinaphar.com/article/view/10101}
}