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作 者:栗俞程[1] 刘亚敏[1] 李阳阳[1] 黄起[1]
出 处:《中华中医药杂志》2014年第10期3229-3231,共3页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:国家自然科学基金(No.81303278);河南中医学院博士科研基金(No.BSJJ2010-24);河南省教育厅自然科学基金(No.12B310004)~~
摘 要:目的:探讨黄芩总黄酮对强迫游泳(FST)小鼠肝脏谷胱甘肽(GSH)、丙二醛(MDA)和超氧化物歧化酶(SOD)含量及血清皮质酮水平的影响。方法:将正常小鼠随机分为5组:正常对照组,FST模型组,阳性药物组(20mg/kg氟西汀),50、100mg/kg黄芩总黄酮组,连续灌胃给药14d。末次给药1h后,除正常对照组外,所有小鼠进行FST实验。摘眼球取血后脱颈椎处死小鼠,分离肝脏、肾脏和脾脏称重,计算脏器指数。试剂盒检测小鼠肝脏GSH、MDA和SOD含量及血清皮质酮水平。结果:黄芩总黄酮对小鼠体质量、肝脏指数、肾脏指数和脾脏指数均无统计学影响;FST小鼠肝脏GSH和SOD含量均显著性减少(P<0.05),MDA含量显著性增高(P<0.05),血清皮质酮水平显著性升高(P<0.001);黄芩总黄酮显著逆转了FST诱导的上述变化(P<0.05)。结论:黄芩总黄酮可增强机体抗应激能力,减轻强迫游泳中的应激行为,抑制下丘脑-垂体-肾上腺(HPA)轴的激活,这可能是其发挥抗抑郁作用的机制之一。Objective: To investigate the effects of flavonoids in scutellaria radix (TFSR) on the contents of glutathione (GSH), malondialdehyde (MDA) and superoxide dismutase (SOD) in mice liver and the corticosterone (CORT) level in mice serum exposed to forced swimming (FST). Methods: The mice were randomly divided into 5 groups: normal control group, FST model group, fluoxetine group (20mg/kg), lower dose TFSB group (50mg/kg) and higher dose TFSB group (100mg/kg). Except for the normal control group, the other groups were succesively gavaged for 14 days. Except for normal control group, the others were conducted FST test after one hour of gavage. All mice were sacrificed after collecting the blood. The fiver, kidney and spleen of mice were weighted to calculate the visceral indexes. The contents of GSH, MDA and SOD in mice liver and the CORT level in mice serum were detected by specific commercial kits respectively. Results: TFSR had no effect on the body weight, liver index, kidney index and spleen index of mice in a state of hepatic oxidative stress caused by forced swimming test. The contents of GSH and SOD in FST model group were both lower than those in other groups (P〈0.05). The content of MDA in FST model group was significant higher than that in other groups (P〈0.05), as well the level of CORT in serum (P〈0.001). And the TFSR significantly reversed all above changes induced by FST (P〈0.05). Conclusion: TFSR can enhance the ability to resist stress, relieve the stress response in FST, and inhibit the activity of HPA axis, which may reveal the key mechanism of its antidepressant effect.
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