Abstract
The increase of blood pressure is accompanied by the changes in the morphology and function of vascular endothelial cells. Vascular endothelial injury and hypertension actually interact as both cause and effect. A large number of studies have proved that inflammation plays a significant role in the occurrence and development of hypertension, but the potential mechanism between inflammation and hypertensive endothelial injury is still ambiguous. The purpose of this study was to explore the association between the activation of NLRP3 inflammasome and hypertensive endothelial damage, and to demonstrate the protective effect of sinapine thiocyanate (ST) on endothelia in hypertension. The expression of NLRP3 gene was silenced by tail vein injection of adeno-associated virus (AAVs) in spontaneously hypertensive rats (SHRs), indicating that activation of NLRP3 inflammasome accelerated hypertensive endothelial injury. ST not only protected vascular endothelial function in SHRs by inhibiting the activation of NLRP3 inflammasome and the expression of related inflammatory mediators, but also improved AngII-induced huvec injury. In summary, our results show that alleviative NLRP3 inflammasome activation attenuates hypertensive endothelial damage and ST ameliorates vascular endothelial dysfunction in hypertension via inhibiting activation of the NLRP3 inflammasome.
Highlights
Hypertension is a multifactorial cardiovascular syndrome with progressive functional or organic impairment, and it is one of the most common chronic diseases worldwide (Doyle, 1991; Elliott, 2007; Scheltens et al, 2010)
Endothelial dysfunction contributes to hypertension, and previous studies have found that elevated blood pressure was accompanied by increased levels of the nucleotide-binding leucine-rich repeat receptor pyrin domaincontaining-3 (NLRP3) inflammasome (Wang et al, 2018a)
There was an imbalance between vasoconstrictors and vasodilators released by the endothelia, which indicated that hypertension is characterized by excessive vasoconstriction induced by vascular endothelial dysfunction
Summary
Hypertension is a multifactorial cardiovascular syndrome with progressive functional or organic impairment, and it is one of the most common chronic diseases worldwide (Doyle, 1991; Elliott, 2007; Scheltens et al, 2010). Increasing research on the pathogenesis of hypertension has revealed that hyperactivity of the sympathetic nervous system and renin-angiotensin aldosterone system (RAAS), water-sodium retention caused by the kidney, insulin resistance, and cell membrane permeability changes are involved in the occurrence and development of hypertension (Zhang et al, 2019). Studies have shown that the occurrence and development of hypertension is accompanied by the involvement of inflammatory factors, among which the nucleotide-binding leucine-rich repeat receptor pyrin domaincontaining-3 (NLRP3) inflammasome is intricately involved in the pathogenesis of hypertension. Inhibiting NF-κB activity reduced NLRP3 and IL-1β levels, thereby reducing hypertension (Qi et al, 2016). These studies suggest that the NLRP3 inflammasome is related to the occurrence and development of hypertension. Their study provides a proof-of-concept that the pharmacological inhibition of the NLRP3 inflammasome is a viable anti-hypertensive strategy (Krishnan et al, 2019)
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