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紫草素对缺血性脑卒中的抗氧化作用OA

Antioxidant Effect of Shikonin on Ischemic Stroke

中文摘要英文摘要

目的 研究紫草素(SKI)对缺血性脑卒中(IS)大鼠的抗氧化作用及其机制.方法 80只SD大鼠依据随机数字表随机分为假手术组、模型组、SKI组和尼莫地平组,每组20只,药物干预3 d后,建立大脑中动脉梗死大鼠模型.SKI组给予SKI 25 mg/kg,尼莫地平组给予尼莫地平10.8 mg/kg,假手术组和模型组给予等体积的生理盐水溶液,给药方式为腹腔注射,1次/d,连续3 d.采用Longa方法对所有大鼠进行神经功能缺损评分;TTC染色检测脑梗死体积;尼氏染色检测缺血半暗带、海马区神经元形态;利用探针DCFH-DA进行脑组织活性氧(ROS)检测;TBA法检测血清丙二醛(MDA)含量;羟胺法检测血清中的总超氧化物歧化酶(T-SOD)含量;ABTS法检测血清中的总抗氧化能力(T-AOC);Western blot检测缺血侧脑组织中Nrf2、HO-1蛋白含量.结果 与假手术组比较,模型组神经功能受损严重、脑梗死体积显著扩大、血清MDA水平升高(P<0.05),神经元排列紊乱,尼氏小体减少甚至消失,血清T-SOD和T-AOC含量下降、脑组织Nrf2、HO-1的蛋白表达均下降(P<0.001);与模型组比较,SKI组神经功能受损明显改善、脑梗死体积缩小(P<0.01),血清MDA水平降低(P<0.05),神经元胞浆、胞核清晰,尼氏体排列整齐,血清T-SOD和T-AOC含量增加、脑组织Nrf2、HO-1的蛋白表达均增加(P<0.01);与尼莫地平组比较,SKI组神经功能损伤评分降低、脑梗死体积减少、血清MDA水平下降(P<0.05),神经元形态恢复并显示出相对有序的排列,尼氏体变得更清晰,血清T-SOD和T-AOC含量增加(P<0.05,P<0.01)、脑组织Nrf2、HO-1的蛋白表达增加(P<0.05).结论 SKI对IS的保护可能是通过调控Nrf2/HO-1信号通路减少脑组织的氧化损伤来发挥作用.

Objective To study the antioxidant effect and mechanism of shikonin(SKI)on ischemic stroke(IS)rats.Methods Eighty SD rats were divided into sham-surgery group,model group,SKI group and nimodipine group(20 for each group)according to the random number table.After 3 days of drug intervention,the rat model of middle cerebral artery occlusion(MCAO)was established.Rats in SKI group were administered SKI at a dose of 25 mg/kg,rats in nimodipine group were administered nimodipine at a dose of 10.8 mg/kg,rats in sham-surgery group and model group were administered an equal volume of physiological saline.Administration was via intraperitoneal injection once a day for 3 days.All rats were scored for neurological deficits by the Longa method;cerebral infarct volume was assessed by TTC staining;neuronal morphology in the ischemic semidorsal zone and hippocampal region was detected by Niehl's staining;brain tissue Reactive Oxygen Species(ROS)was detected by the probe DCFH-DA;serum Malondialdehyde(MDA)content was detected by the TBA method;Total Superoxide Dismutase(T-SOD)content in serum was detected by hydroxylamine method;Total Antioxidant Capacity(T-AOC)in serum was detected by ABTS method;Western Blot was employed to detect Nrf2 and HO-1protein content in the brain tissue on the ischaemic side.Results Compared with the sham-surgery group,the model group showed severe neurological impairment,significantly enlarged cerebral infarction volume,increased serum MDA level(P<0.05),disorganised neuronal arrangement,reduced or even disappeared Nissl bodies,decreased serum T-SOD and T-AOC levels,and decreased protein expression of Nrf2 and HO-1 in brain tissue(P<0.001).Compared with the model group,the SKI group showed significant improvement in impaired neurological function,reduction in cerebral infarction volume(P<0.01)and serum MDA level(P<0.05),clear neuronal cytoplasm and nuclei,well-arranged Nissl bodies,and increased expression of serum T-SOD and T-AOC content,and protein content of Nrf2 and HO-1(P<0.01).Compared with the nimodipine group,the SKI group showed a lower neurological impairment score,decreases in cerebral infarction volume,serum MDA level(P<0.05),neuronal morphology was restored and showed a relatively well-ordered arrangement,the Nissl bodies became more well-defined,the serum T-SOD level(P<0.05)and T-AOC level(P<0.01)were increased,and protein content expression of brain tissues of Nrf2,HO-1 increased(P<0.05).Conclusion The protective effect of SKI against IS may be attributed to the reduction of oxidative damage in brain tissue via the regulation of the Nrf2/HO-1 signaling pathway.

荆文馨;林强;符瑶;龙欣悦;李琦;王岚宁;宿海超;杨春壮

牡丹江医科大学,黑龙江 牡丹江 157011牡丹江医科大学附属红旗医院,黑龙江 牡丹江 157000牡丹江医科大学,黑龙江 牡丹江 157011牡丹江医科大学,黑龙江 牡丹江 157011牡丹江医科大学,黑龙江 牡丹江 157011牡丹江医科大学,黑龙江 牡丹江 157011牡丹江医科大学附属红旗医院,黑龙江 牡丹江 157000牡丹江医科大学,黑龙江 牡丹江 157011

缺血性脑卒中紫草素抗氧化Nrf2/HO-1信号通路

Ischemic strokeShikoninAntioxidantNrf2/HO-1 signal pathway

《中医药信息》 2026 (2)

11-17,7

黑龙江省省属高等学校基本科研业务费科研项目(2023-KYYWF-0938)

10.19656/j.cnki.1002-2406.20260203

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