香芹酚通过抑制脑水肿与氧化应激反应保护大鼠颅脑损伤

Carvacrol protects against traumatic brain injury in rats through suppressing the brain edma and oxidative stress

目的探讨香芹酚对大鼠颅脑损伤(TBI)的保护作用及其机制。方法 SD大鼠50只,随机分为5组:假手术组、模型组、低剂量香芹酚(10 mg/kg)组、中剂量香芹酚(20 mg/kg)组、高剂量香芹酚(40 mg/kg)组,每组10只。Feeney氏自由落体法制备TBI模型,造模后1、3、7 d采用改良神经功能损害程度评分(m NSS)评估神经功能,干湿法测定脑组织含水量;ELISA法检测氧化应激因子丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、过氧化氢酶(CAT)以及化学定量法检测一氧化氮(NO)含量及一氧化氮合酶(NOS)活性。结果香芹酚能显著改善大鼠TBI后神经功能,显著减轻TBI后脑水肿,显著降低损伤脑组织MDA、NO和NOS含量,显著增加损伤脑组织SOD、CAT和GSH含量。结论香芹酚可通过减轻大鼠TBI后脑水肿、抑制氧化应激从而发挥神经保护作用。

Objective To investigate the effect of carvacrol on trauma-injured brain and its mechanism in rats. Methods Animal models of traumatic brain injury was established by Freeney free-falling method in 40 SD rats, which were randomly divided into 4 groups of 10 animals each, including control group, experimental group A, in which each rat received the intraperitoneal injection of 10 mg/kg of carvacrol every day for 7 days, experimental group B, in which each rat did injection of 20 mg/kg, the experimental group C, in which each rat did injection of 40 mg/kg. The other 10 rats underwent sham operation in sham group. The neurological functions were evaluated by modified neurological severity score （mNSS） in all the groups 1, 3 and 7 days after the injury. The water content in the injured cerebral tissues was determined 7 days after the injury. The contents of malondialdehyde （MDA）, catalase （CAT）, superoxide dismutase （SOD）,and glutathione （GSH） in the injured brain tissues were detected by ELISA and the content of NO and the activity of NO synthase （NOS） in the injured cerebral tissues were measured 7 days after the injury. Results The mNSS and water contents in the injured cerebral tissues significantly decreased in all the experimental groups compared to those in the control group （P〈0.05）. MDA, CAT, SOD and GSH activities in the injured cerebral tissues significantly decreased in carvacrol groups compared with those in the control group 7 days after the injury （P〈0.05）. The content of NO and the activity of NOS in the injured cerebral tissues were significantly lower in all the experimental groups than those in the control group （P〈0.05）. Conclusions It is suggested that carvacrol protects trauma-injured brain probably through suppressing the brain edema and oxidative stress.