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作 者:宋春林 龚方 刘伍才 袁金华 曾宪晶 SONG Chunlin;GONG Fang;LIU Wucai;YUAN Jinhua;ZENG Xianjing(Department of General Practice,Affiliated Hospital of Jinggangshan University,Jiangxi Province,Ji'an 343000,China;Department of Oncology,Jishui County People's Hospital,Jiangxi Province,Ji'an 343000,China)
机构地区:[1]井冈山大学附属医院全科,江西吉安343000 [2]吉水县人民医院肿瘤科,江西吉安343000
出 处:《光明中医》2023年第11期2101-2103,2191,共4页GUANGMING JOURNAL OF CHINESE MEDICINE
基 金:国家自然科学基金项目(No.81460725);江西省中医药管理局科技计划项目(No.2022A341);江西省吉安市指导性科技计划项目(No.2022-16号)。
摘 要:目的 探讨清热化瘀方对急性脑缺血损伤大鼠的神经保护作用机制。方法 将SD大鼠分为假手术组,缺血模型组,清热化瘀方低中高剂量组,每组10只,参照MCAO术造模,假手术组和模型组均予生理盐水灌胃,清热化瘀方剂量组予不同剂量清热化瘀汤灌胃。术后对大鼠进行神经功能缺损评分,神经元HE染色,TUNEL检测凋亡细胞,Western-blot检测脑组织自噬与凋亡蛋白水平。结果 与模型组比较,清热化瘀方组神经功能评分明显下降(P<0.05),清热化瘀方组神经元整体病理损伤减轻,TUNEL凋亡阳性细胞比例下降(P<0.05),清热化瘀方组Beclin-1和LC3蛋白表达量上升,Caspase-3蛋白表达水平下降(P<0.05)。结论 清热化瘀方可能通过调节凋亡与自噬水平而发挥了神经保护作用。Objective To explore the protective mechanism of clearing heat and removing blood stasis recipe on acute cerebral ischemia injury in rats.Methods SD Rats were divided into sham operation group,ischemia model group,low,middle and high dose group of clearing heat and removing blood stasis recipe,with 10 rats in each group.According to the model of MCAO,the Qingre Huayu group was given different doses of Qingre Huayu decoction,the sham-operation group and the model group were given normal saline.After the operation,the rats were scored for neurological deficit,the neurons were stained by HE,TUNEL detection of apoptotic cells,the levels of apoptosis and autophagy protein phosphorylation were detected by Western-blot.Results Compared with the model group,the score of nerve function in the Qingre Huayu group decreased significantly(P<0.05),the overall pathological damage in the Qingre Huayu group decreased,the proportion of TUNEL positive cells in the Qingre Huayu group decreased(P<0.05),the expression of Beclin-1 and LC3 protein increased,and the expression of Caspase-3 protein decreased(P<0.05).Conclusion Clearing heat and removing blood stasis recipe can alleviate cerebral ischemia injury by regulating apoptosis and autophagy.
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