田蓟苷对脑缺血再灌注损伤模型大鼠脑组织的保护作用研究
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篇名: 田蓟苷对脑缺血再灌注损伤模型大鼠脑组织的保护作用研究
TITLE:
摘要: 目的:研究田蓟苷(TIL)对脑缺血再灌注损伤模型大鼠脑组织的保护作用。方法:120只雄性SD大鼠随机分为假手术组(0.9%氯化钠溶液)、模型组(0.9%氯化钠溶液)、尼莫地平组(32 mg/kg)和TIL低、中、高剂量组(4、8、16 mg/kg),每组20只。灌胃相应药物,每天1次,连续7 d,末次给药15 min后,以改良线栓法建立脑缺血再灌注损伤模型。进行大鼠神经功能缺损评分;计算大鼠脑梗死体积百分比;采用苏木精-伊红染色法观察大鼠脑组织病理形态学;检测大鼠脑组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、乳酸脱氢酶(LDH)活性和丙二醛(MDA)含量;采用Western blot法检测大鼠脑组织中降钙素基因相关肽(CGRP)、血管内皮细胞生长因子受体2(VEGFR2)蛋白表达。结果:与假手术组比较,模型组大鼠神经功能缺损评分显著升高(P<0.01);脑组织梗死体积百分比显著升高(P<0.01);脑组织神经细胞明显缩小变形,细胞间质水肿明显;脑组织中SOD、CAT活性均显著减弱,LDH活性显著增强,MDA含量显著增加,CGRP、VEGFR2蛋白表达均显著增强(P<0.05或P<0.01)。与模型组比较,尼莫地平组和TIL中、高剂量组大鼠神经功能缺损评分均显著降低(P<0.05或P<0.01);脑组织梗死体积百分比均显著降低(P<0.05或P<0.01);脑组织上述病理改变均明显减轻;脑组织中SOD、CAT活性均显著增强,LDH活性均显著减弱,MDA含量均显著减少,CGRP、VEGFR2蛋白表达均显著增强(P<0.05或P<0.01)。结论:TIL对脑缺血再灌注损伤模型大鼠脑组织具有一定保护作用,其机制可能与上调CGRP和VEGFR2表达有关。
ABSTRACT: OBJECTIVE: To study the effects of tilianin(TIL) on brain tissue in rats with cerebral ischemia-reperfusion injury. METHODS: Totally 120 male SD rats were randomly divided into sham operation group (0.9% sodium chloride solution), model group (0.9% sodium chloride solution), nimodipine group (32 mg/kg) and TIL low-dose and medium-dose, high-dose groups (4, 8, 16 mg/kg), with 20 rats in each group. The rats were given relevant medicine intragastrically, once a day, for consecutive 7 d. 15 min after last medication, cerebral ischemia-reperfusion injury model was established by reforming suture-occluded method. The neurological deficit score in rats were evaluated, and percentage of cerebral infarction volume of rats was determined. Histopathological changes of brain tissue were observed by HE staining. The activities of SOD, CAT and LDH, MDA content in cerebral tissue of rats were determined. The expression of calcitonin gene-related peptide (CGRP) and peripheral vascular endothelial growth factor receptor 2 (VEGFR2) protein were determined by Western blot assay. RESULTS: Compared with sham operation group, neurological deficit score and percentage of cerebral infarction volume of model group were increased significantly (P<0.01); the nerve cells in brain tissue were significantly reduced and the interstitial edema was obvious. SOD and CAT activities were decreased significantly, LDH activity was increased significantly, MDA content was decreased significantly,protein expression of CGRP and VEGFR2 were increased significantly (P<0.05 or P<0.01). Compared with model group, neurological deficit score of nimodipine group, TIL medium-dose and high-dose groups were decreased significantly; percentage of cerebral infarction volume was decreased significantly (P<0.05 or P<0.01); above pathological conditions of cerebral tissue in rats were relieved significantly; SOD and CAT activities were strengthened significantly, MDA content and LDH activities were decreased significantly, protein expression of CGRP and VEGFR2 were increased significantly (P<0.05 or P<0.01). CONCLUSIONS: TIL has certain protective effects on cerebral ischemia-reperfusion injury model rats, and its mechanism may be related to the up-regulation of CGRP and VEGFR2 expression.
期刊: 2018年第29卷第20期
作者: 马丽月,曾诚,郑瑞芳,姜雯,何承辉,邢建国
AUTHORS: MA Liyue,ZENG Cheng,ZHENG Ruifang,JIANG Wen,HE Chenghui,XING Jianguo
关键字: 田蓟苷;脑缺血再灌注损伤;降钙素基因相关肽;血管内皮细胞生长因子受体2;保护作用
KEYWORDS: Tilianin; Cerebral ischemia-reperfusion injury; CGRP; VEGFR2; Protection
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