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Chinese Pharmaceutical Journal ; (24): 1589-1593, 2015.
Article in Chinese | WPRIM | ID: wpr-859615

ABSTRACT

OBJECTIVE: To investigate the inhibitory effect of ginsenoside Re on vascular neointimal hyperplasia induced by balloon-injury and probe its molecular mechanism in rats. METHODS: The rat carotid artery neointimal hyperplasia model was established by rubbing the endothelia with a balloon in male Sprague-Dawley rats, then animals were intrapritoneally injected with distilled water in model group and sham operation group or with ginsenoside Re 6, 12 and 24 mg·kg-1·d-1 in other endothelia rubbed groups. After 14 consecutive days, the injuried artery was taken for H&E staining, the histopathological observation and detecting the neointimal area as well as the ratio of neointimal area/media area were taken to evaluate the vescular intimal hyperplasia level. For probing the molecular mechanism, the expression of mitogen-activated protein kinase phosphatase-1 (MKP-1) was detected at the transcript levels by real time RT-PCR, and the protein expressions of MKP-1 and phosphorylation extracellular signal-regulated kinase 1/2 (pERK12) were examined by immunohistochemistry and analyzed with Image-Pro Plus. RESULTS: Compared with the endothelia rubbing model group, ginsenoside Re 6, 12, 24 mg·kg-1·d-1 medications significantly improved the histopathological changes induced by baloon-injury, decreased the elevated neointimal area and the ratio of neointimal area/media area induced by baloon-injury; ginsenoside Re administration could also down-regulate the elevated pERK1/2 protein expression, and significantly up-regulated the decreased MPK-1 mRNA and protein expressions induced by baloon-injury. CONCLUSION: Ginsenoside Re inhibits the vascular neointimal hyperplasia induced by baloon-injury in rats, the molecular mechanism is related to its inhibition effect on ERK signaling.

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