Effects of Sapindus saponin on vascular endothelial function and NLRP3 inflammasome in spontaneously hypertensive rats
AIM To investigate the effects of Sapindus saponin on vascular endothelial function and nucleotide binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome in spontaneously hypertensive rats.METHODS In contrast to the 6 WKY rats of the control group treated with normal saline,other 18 spontaneously hypertensive rats(SHR)were divided into the model group for normal saline treatment,the Sapindus saponin group and the telmisartan group for the corresponding treatment at concentration of 162 mg/kg and 10 mg/kg,respectively,for a 35-day programme,with 6 rats in each group.The rats had their expression of von Willebrand factor(vWF)in the intima of thoracic aorta detected by immunohistochemistry;their pathological changes of thoracic aorta observed by HE staining;their serum levels of cysteinyl aspartate specific proteinase 1(caspase-1)and interleukin 1β(IL-1β)detected by ELISA;and their mRNA and protein expressions of p38,NLRP3,and caspase-1 in aortic tissues detected by RT-qPCR and Western blot.RESULTS Compared with the control group,the model group displayed increased SBP and DBP levels in tail artery,serum caspase-1 and IL-1β levels,and mRNA and protein expressions of p38,NLRP3 and caspase-1 in thoracic aorta(P＜0.01);increased positive expression of vWF in the thoracic aortic intima(P＜0.01),severe loss of aortic intima and adventitia,and thickening of the media.Compared with the model group,the Sapindus saponin and telmisartan groups shared decreased SBP and DBP levels in the tail artery,serum caspase-1 and IL-1β levels,and the mRNA and protein expressions of p38,NLRP3 and caspase-1 in the thoracic aorta(P＜0.05),reduced positive expression of vWF in the thoracic aortic intima(P＜0.05),reduced damage of aortic inner and outer membrane and thickness of the media as well.CONCLUSION Sapindus saponin can effectively reduce the blood pressure,improve the vascular endothelial dysfunction and inhibit the inflammatory response in spontaneously hypertensive rats,and the mechanism may be related to the inhibited activation of NLRP3 inflammatory pathway.
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