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葛根素对大鼠颅脑损伤的保护作用
引用本文:李国亮,邸,方,杨亚东.葛根素对大鼠颅脑损伤的保护作用[J].中国临床神经外科杂志,2016,0(8):479-482.
作者姓名:李国亮      杨亚东
作者单位:430040,武汉市东西湖区人民医院神经外科(李国亮、邸 方);438000 湖北,黄冈市中心医院重症医学科(杨亚东) 通讯作者:杨亚东,E-mail:lglwaike@126.com
摘    要:目的 探讨葛根素对大鼠颅脑损伤(TBI)的保护作用及其机制。方法 将45只SD大鼠随机分为假手术组、模型组、低剂量葛根素组、中剂量葛根素组和高剂量葛根素组,每组9只。采用Feeney氏自由落体法制备TBI大鼠模型。低、中、高剂量葛根素组腹腔注射葛根素,剂量分别为10、25、50 mg/kg。造模后1、3、7 d采用改良神经功能缺损评分(mNSS)评价神经功能。造模后7 d,干湿法测定脑组织含水量;ELISA法检测脑组织丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、过氧化氢酶(CAT)、核因子κB (NF-κB)、细胞间黏附分子-1(ICAM-1)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、caspase-3水平;免疫印迹法检测Bax、Bcl-2的表达。结果 葛根素能显著降低TBI大鼠mNSS(P<0.05),显著减轻脑组织水肿(P<0.05),显著降低脑组织MDA、SOD、GSH、CAT、NF-κB、ICAM-1、IL-6、TNF-α、caspase-3水平(P<0.05),显著下调Bax表达而上调Bcl-2表达(P<0.05)。结论 葛根素可通过减轻颅脑水肿、抑制氧化应激及炎性反应以及调节Bax/Bcl-2表达从而发挥神经保护作用。

关 键 词:颅脑损伤  氧化应激  炎症反应  细胞凋亡  大鼠  葛根素

Neuroprotective effects of puerarin on cerebral tissues injured by trauma and its mechanism in rats
LI Guo-liang,DI Fang,YANG Ya-dong..Neuroprotective effects of puerarin on cerebral tissues injured by trauma and its mechanism in rats[J].Chinese Journal of Clinical Neurosurgery,2016,0(8):479-482.
Authors:LI Guo-liang  DI Fang  YANG Ya-dong
Institution:1. Department of Neurosurgery, People's Hospital of Dongxihu District of Wuhan City, Wuhan 430040, China; 2. Intensive Care Unit, Central Hospital of Huanggang City, Huanggang 438000, China
Abstract:Objective To investigate the effect of puerarin on the cerebral tissues injured by trauma and its mechanism in rats. Methods Forty-five SD rats were randomly divided into 5 groups of 9 animals each, i.e. sham operation, brain injury and 10 mg/kg, 25 mg/kg and 50 mg/kg puerarin treatment groups. The animal models of traumatic brain injury were established by Feeney method. Puerarin dose corresponding to the treatment group was intraperitoneally injected once a day for 7 days in all the treatment groups. The neurological functions were evaluated by modified neurological severity scale (mNSS) 1, 3 and 7 days after the injury in all the groups. The water contents in the injured cerebral tissues were determined 7 days after the injury. The expression of malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), nuclear factor-κB (NF-κB), tumor necrosis factor (TNF-α), intercellular cell adhesion molecule-1, interleukin-6 and caspase-3 in the cerebral tissues were detected by ELISA and the expressions of Bax and Bcl-2 protein in the cerebral tissues were detected by Western blot 7 days after the injury. Results The mNSS scores 1, 3 and 7 days after the injury and water contents in the injured cerebral tissues 7 days after the injury were significantly lower in all the treatment groups than those in the brain injury group (P<0.05). The levels of MDA、CAT、SOD and GSH, NF-κB, TNF-α, ICAM-1, IL-6 and caspase-3 expressions were significantly lower 7 days after the injury in all the treatment group than those in the brain injury group (P<0.05). The level of Bax protein expression was significantly lower and level of Bcl-2 protein expression was significantly higher in the cerebral tissues in all those in the brain injury group (P<0.05). Conclusions It is suggested that puerarin protects the cerebral tissues injured by trauma probably through the relief of cerebral edema, inhibition of oxidation-stress action and inflammatory action and regulation of Bcl-2 and Bax expression in the cerebral tissues.
Keywords:Puerarin  Traumatic brain injury  Oxidation-stress action  Inflammatory action
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