慢性束缚应激小鼠海马应激性病理效应

Stressful pathological effects of hippocamal in chronic restraint stress mice

目的观察慢性束缚应激下小鼠海马神经元数目的改变及天冬氨酸特异性半光氨酸蛋白酶-3的活性,探讨应激对海马的损害作用及途径。方法将16只小鼠随机分为对照组和应激组各8只,采用50ml离心管建立慢性束缚应激模型,每晚束缚8min。14d后处死,取小鼠海马常规固定制HE片、免疫组化天冬氨酸特异性半光氨酸蛋白酶-3片,在显微镜下进行细胞记数并显微拍照。结果慢性束缚应激组小鼠海马数目较对照组减少(P<0.05),同时天冬氨酸特异性半光氨酸蛋白酶-3阳性细胞率增加(P<0.05);镜下神经元发生空泡变性,存在典型凋亡细胞。结论慢性束缚应激海马神经元凋亡蛋白天冬氨酸特异性半光氨酸蛋白酶-3活性增加,天冬氨酸特异性半光氨酸蛋白酶-3可能参与了应激状态下海马的细胞凋亡。

Objective To observe changes of hippocamal neurons and activities of Caspase-3 in the hippocampus of chronic restraint stress mice and explore the injuring actions and ways of stress to hippocampus.Methods 16 mice were randomly divided into control and stressful group （both n = 8）, RST devices were constructed with 50-ml polypropylene conical tubes, restrain stress was imposed for 8 minutes per night.After Fourteen days mice were killed and brains were taken.The paraffin section for the He and immunohistochemistry Caspase-3 were routinely made, counts of positive cell and photomicrographs taken under microscope. Results Decrease of hippocamal neurons were more marked in the stress than in the control group（P〈0. 05） and rate of positive cell of Caspase-3 increased more signifieantly（P〈0.05）; Neurons developed vacuolar degeneration and had dead cells.Conclusion Activity of hippocamal Caspase-3 increased and Caspase-3 might play a role in the death of hippocamal neurons under stress.