The Study Of Estrogen And Exercise Protected Mechanism In Myocardium Of Ovariectomized Rats

Part ⅠObjective:Explore the protective mechanism of estrogen on myocardium in ovariectomized rats.Methods:Thirty female SD rats, sham operation control group (Group C), ovariectomy group (OVX group) and estrogen replacement group (OVX+E2 group) according to the weight, estradiol test results and uterine weight determined in ovariectomized rat model was established successfully. A week after treated with abdominal subcutaneous injection of benzoate estradiol 30ug/kg.d, sham operated control group and subcutaneous injection of ovaries were given the same amount of solvent, after three months from left ventricular tissue. Using immunohistochemistry and hydrogen sulfide detection method, the formation of hydrogen sulfide in the detection of myocardial and determine the CSE expression by RT-PCR and Western blot method, detected in CSE expression, using ELISA detection method, detection of oxidative stress indexes GSH/GSSG, T-AOC, cat, SOD activity and proinflammatory IL-6 and TNF-a level.Results:1 CSE was expressed in the myocardium.2 estrogen can up regulate the expression of CSE in the myocardium of ovariectomized rats (P< 0.05).3 the effect of estrogen in the myocardium (P< 0.05).4 the ability of estrogen in the myocardium to enhance the pro-inflammatory factor (P< 0.05).5.H2S and ovariectomized rats myocardial promoting of TNF alpha and IL-6 activity showed a negative correlation (P< 0.05), and the ratio of GSH/GSSG and T-AOC was positive correlation (P< 0.05), but and the activity of SOD and cat no correlations (P> 0.05).Conclusion:estrogen replacement can increase the expression of CSE in the myocardium of OVX rats and promote the generation of endogenous hydrogen sulfide gas.. Secondly, estrogen can increase the ability of resistance to oxidative stress and inflammation, and correlation analysis pointed out that the endogenous hydrogen sulfide gas and anti oxidative stress indicators were positively correlated and proinflammatory factor showed a negative correlation, suggesting that we estrogen mechanism of myocardial protection by promoting CSE expression, and increased resistance to oxidative stress and inflammation ability, eventually played the role of myocardial protection.Part ⅡObjective:To explore the protective mechanism of exercise on the myocardium in ovariectomized rats.Methods:Forty female SD rats, sham operation control group (Group C) and sham operation movement exercise group (SHAM+EX group), to ovariectomy (OVX group) and exercise for the alternative group (group OVX+EX), according to the weight, estradiol test results and uterine weight determined in ovariectomized rat model was established successfully. A week after surgery, the intensity of the exercise (18m/min, sustained 1h/d, 6d/weeks), three months after the left ventricular tissue. Using RT-PCR and Western blot method, detected in CSE expression and estrogen receptor ER-a and ERbeta was content, using ELISA detection method, detection of oxidative stress indexes of MDA activity, T-AOC, cat and SOD activity.Results:1. Exercise can increase the expression of CSE in myocardium of OVX rats (P< 0.05).2.Exercise improve the T-AOC ability of the antioxidant stress index in the myocardium, and decrease the activity of MDA (P< 0.05).3.In the myocardium estrogen receptor ER-a was expressed (P< 0.05), but the estrogen receptor ER-p had no change (P> 0.05) with CSE level and antioxidant stress indexes of T-AOC was positively correlated (P< 0.05), and MDA activity a negative correlation (P< 0.05), and estrogen receptor ER-a positive correlation (P< 0.05), the estrogen receptor ER-β no correlation with CSE level.Conclusion:We find that exercise can increase the level of CSE in ovariectomized rats myocardial, and may enhance oxidative stress index T-AOC level and decrease the level of MDA in the OVX group myocardium. Exercise can increase estrogen receptor a level in myocardium. This suggests that we can enhance the myocardial antioxidant and inflammatory effect by adjusting the CSE/H2S pathway, and ultimately protect the myocardia.