Abstract: Objective：To observe the regulation of estrogen on the expressions of Monocyte chemotactic factor 1 (MCP-1) and Ras homolog gene family member A (RhoA) in female ovariectomized Sprague-Dawley rats, so as to study the protective effect of estrogen on cardiovascular system. Methods: Forty five female rats aged 12 weeks were randomly divided into five groups: the blank control group (CON, n=10), the ovariectomized group (OVX, n=12), the estrogen-treated group with 17β-estradiol (OVX+E2, n=13) and the sham-operated group (SHAM, n=10). 200 μg/(kg·d) 17β-estradiol was administered in the OVX+ E2 group for 16 weeks, the other three groups were given equal normal saline. After 16 weeks, the levels of serum estradiol (E2), follicle-stimulating hormone (FSH), monocyte chemotactic factor 1 (MCP-1) and RhoA were measured by ELISA; the heart tissue was harvested and weighted, the morphological change was observed by HE staining. The levels of tissue silence regulating protein 1 (SIRT1), activated protein kinase (AMPK) were measured by ELISA. The expressions of MCP-1 and RhoA were detected by immunofluorescence histochemistry. Results: The levels of serum and heart tissue RhoA and MCP-1 in the OVX+E2 group were significantly lower than those in the OVX group (P＜0.05). The levels of heart tissue SIRT1 and AMPK in the OVX+E2 group were significantly higher than those in the OVX group (P＜0.05). Conclusions: The estrogen replacement plays a protective effect in those female ovariectomized rats by down-regulating the expressions of serum and heart tissue MCP-1 and RhoA. The potential mechanism is that the AMPK/SIRT1 pathway may be up-regulated by 17β-estradiol.

Key words:  Estradiol, Silence regulating protein 1, AMP-activated protein kinase, Monocyte chemotactic factor 1, Ras homolog gene family, member A, Animal experimentation