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目的 研究余甘子提取物对大鼠局灶性脑缺血再灌注损伤的保护作用及机制.方法 大鼠随机分为假手术组,模型组,余甘子提取物高、中、低剂量(生药6.0、3.0、1.5 g/kg)组和阳性药组(银杏叶提取物100 mg/kg),各给药组每天ig给药1次,连续给药10 d.末次给药后30 min,大脑中动脉线栓法制备大鼠脑缺血再灌注模型,造模后,行神经功能学评分,测定脑梗死面积和脑组织超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、诱导性一氧化氮合酶(iNOS)、核转录因子(NF-κB)的水平.结果 与模型组相比,余甘子提取物能减少局灶性脑缺血再灌注大鼠的神经功能评分和脑梗死面积(P<0.05),提高脑组织SOD活性(P<0.05),降低MDA、NO、IL-1β、IL-6、iNOS和NF-κB的水平(P<0.05).结论 余甘子提取物对大鼠脑缺血再灌注损伤具有明显的保护作用,其机制可能与抗氧化和抑制炎症有关.
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[Abstract]
Objective To study the protection of extract from Phyllanthus emblica (EPE) on focal cerebral ischemia-reperfusion injury in rats and its mechanism. Methods Male SD rats were divided into six groups such as Sham, model, Ginkgo biloba extract (100 mg/kg, positive control), low-, mid-, and high-dose (crude drug 6.0, 3.0, and 1.5 g/kg) EPE groups. The rats in the treatment groups were ig administered once daily for 10 d. On day 10 the focal cerebral ischemia-reperfusion rat model was established using middle cerebral artery occlusion method. After the model establishment, the neurological function scores were observed, the infarct size was measured by TTC staining, and the contents of SOD, MDA, NO, IL-1β, IL-6, iNOS, and NF-κB in brain tissue were measured. Results Compared with the model group, EPE could significantly reduce the neurological function scores (P < 0.05), decrease the cerebral infarct size (P < 0.05), increase the activity of SOD (P < 0.05), and reduce the contents of MDA, NO, IL-1β, IL-6, iNOS, and NF-κB (P < 0.05) in brain tissue. Conclusion EPE has the significant protection on cerebral ischemia-reperfusion injury in rats due to increasing the anti-oxidant activity and inhibiting the inflammatory reaction.
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