Key Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Collaborative Innovation Center of Chinese Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; Department of Pharmacology, School of Pharmacy, Zunyi Medical University, Zunyi, Guizhou 563000, China.
Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, China; The Key Laboratory of Chemistry for Natural Products of Guizhou Province and Chinese Academic of Sciences, Guiyang, Guizhou 550014, China.
Biomed Pharmacother. 2023 Jul;163:114843. doi: 10.1016/j.biopha.2023.114843. Epub 2023 May 16.
Calcium-sensing receptor (CaSR) is a G protein-coupled receptor, widely distributed in various tissues, including vascular endothelial cells and smooth muscle cells, which plays an important role in the migration and homing of stem/progenitor cells and the proliferation of tissue cells. Restenosis after Percutaneous coronary intervention (PCI) seriously affects its prognosis and application. Our previous research has found that ginsenoside Rg1 (GS-Rg1) can inhibit the occurrence of restenosis after balloon injury of the common carotid artery in rats, but the mechanism is still unclear. In this study, it was found that GS-Rg1 (4, 8, 16 mg/kg) inhibited vascular restenosis caused by balloon injury, and mobilize endothelial progenitor cells (EPCs) to promote reendothelialization and inhibit intimal hyperplasia, which significantly reduced after administration of CaSR antagonist NPS 2143. Interestingly, CaSR and its downstream JNK, P38 were highly expressed in the proliferative intima and participated in the abnormal proliferation of vascular smooth muscle cells mediated by smooth muscle progenitor cells (SMPCs). GS-Rg1 inhibited intimal hyperplasia, while it decreased the expression of CaSR, JNK, and P38. This might relate to the distribution of CaSR and the facilitation of GS-Rg1 on the vascular endothelial repair. It is concluded that CaSR plays a key role in GS-Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon Injury.
钙敏感受体（CaSR）是一种 G 蛋白偶联受体，广泛分布于多种组织中，包括血管内皮细胞和血管平滑肌细胞，在干细胞/祖细胞的迁移和归巢以及组织细胞的增殖中发挥重要作用。经皮冠状动脉介入治疗（PCI）后的再狭窄严重影响其预后和应用。我们之前的研究发现，人参皂苷 Rg1（GS-Rg1）可抑制大鼠颈总动脉球囊损伤后再狭窄的发生，但机制尚不清楚。本研究发现，GS-Rg1（4、8、16mg/kg）可抑制球囊损伤引起的血管再狭窄，动员内皮祖细胞（EPCs）促进再内皮化和抑制内膜增生，明显降低 CaSR 拮抗剂 NPS 2143 给药后的再狭窄。有趣的是，CaSR 及其下游 JNK、P38 在增殖内膜中高表达，并参与平滑肌祖细胞（SMPCs）介导的血管平滑肌细胞异常增殖。GS-Rg1 抑制内膜增生，同时降低 CaSR、JNK 和 P38 的表达。这可能与 CaSR 的分布以及 GS-Rg1 对血管内皮修复的促进作用有关。综上所述，CaSR 在 GS-Rg1 促进再内皮化抑制球囊损伤后内膜增生中起关键作用。
