In recent years, menopausal syndrome has attracted much attention.According to epidemiological survey, women after menopause neurodegenerative disease incidence increased significantly. With Alzheimer’s Disease as an example, the incidence of postmenopausal women is 2 to 3 times higher than men of the same age. Hormone replacement therapy can supply estrogen for menopausal women. Studies showed that hormone replacement therapy could reduces the risk of AD,delay the onset AD, and improve cognitive function. In addition a large number of animal experiments and clinical trials also confirmed that estrogen had curative effect for a variety of neurodegenerative diseases.Neuron apoptosis is one of the important pathologic character of neurodegenerative diseases. Study indicates that cell apoptosis mainly through four death signal pathways. They are the death receptor-mediated extrinsic pathway, mitochondrial pathway, granzyme B-mediated pathway and endoplasmic reticulum stress-mediated pathway. In mitochondrial pathway Bcl-2 family plays an improtant role. Bcl-2 family includes two categories, among them Bcl-2, Bcl-xl and Bcl-w can inhibit cell apoptosis,as Bax, Bid and Bak can promote apoptosis. This experiment is intended to explore the mechanism of estrogen protect neurons through mitochondrial pathway by Bax, Bcl-2 and apoptosis inducing factor.8 weeks female C57 mice were randomly grouped into control group,sham-operated group, ovariectomized group and estradiol treated group.The ovariectomized group and estradiol treated group were ovariectomized bilaterally. Observing vaginal smear tested the modle.After 6 weeks later the estradiol treated group were injected with estradiol2 weeks, while others treated with blank reagent. The serum levels of estrogen were determined by ELISA. Immunohistochemistry and Western blot were used to evaluate the expression of Bax, Bcl-2 and AIF in brains.Compared with control group, sham-operated group, estradiol treated group, the serum levels of estrogen were low in ovariectomized group.While there was no significantly difference of estrogen level in sham-operated group, control group and estradiol treated group. The expressions of Bax, AIF in ovariectomized group were significantly higher than sham-operated group, control group and estradiol treated group.While, the expresstion of Bcl-2 and the ratio of Bcl-2/Bax in ovariectomized group were lower than sham-operated group, control group and estradiol treated group.Estrogen decrease could accelerate the apoptosis of neurons.Supplying estradiol on the menopause mice could improve the effect. Bax,Bcl-2, AIF involved in the mitochondrial pathway participated in this process. |