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(m NSS)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m NSS(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。
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 clay 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-K B (NF-K B), tumor necrosis factor (TNF-ot), intercellular celt adhesion molecule-l, 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 clays 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.
出处
《中国临床神经外科杂志》
2016年第8期479-482,共4页
Chinese Journal of Clinical Neurosurgery
关键词
颅脑损伤
氧化应激
炎症反应
细胞凋亡
大鼠
葛根素
Puerarin
Traumatic brain injury
Oxidation-stress action
Inflammatory action