摘要
目的:探究丹酚酸B(SalB)对局灶性脑缺血再灌注大鼠脑组织血管生成、氧化应激反应的影响以及对脑组织损伤的保护作用。方法:将40只SD大鼠分成4组:健康组(Ctrl);加药组:健康大鼠腹腔注射丹酚酸B50mg/kg体重;模型组:参考文献建立局灶性脑缺血再灌注(MCAO)大鼠模型;模型加药组(MCAO+SalB):在建模前3d向大鼠腹腔注射SalB50mg/kgBW,每天1次,再灌注后2h给药;各组大鼠在建模后24h处死。苏木素伊红(HE)染色检测各组大鼠脑组织病理损伤。TUNEL染色检测脑组织细胞凋亡。试剂盒检测丙二醛(MDA)、超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)的含量。免疫组化检测细胞间黏附分子-1(ICAM-1)的表达情况。Westernblot检测血管内皮生长因子(VEGF)及其受体VEGFR2的表达,检测p38、Hsp27的磷酸化水平。结果:与对照组相比,模型组大鼠脑组织出现显著的组织病变;凋亡细胞比率明显升高(P<0.01);SOD含量明显下降,MDA和LDH的含量明显上升(P<0.01);ICAM-1的表达显著上调(P<0.01);VEGF及受体分子VEGFR2的表达显著下调(P<0.01);p38和Hsp27的磷酸化水平显著降低(P<0.01)。模型加药组与模型组相比较,大鼠脑组织病理损伤明显减轻;凋亡细胞显著减少(P<0.01);SOD含量显著上升,MDA和LDH的含量显著下降(P<0.01);ICAM-1蛋白表达显著下调(P<0.01);VEGF和VEGFR2的表达显著上调(P<0.01);p38和Hsp27的磷酸化水平显著提高(P<0.01)。结论:丹酚酸B可能通过诱导血管新生、缓解氧化应激反应,对局灶性脑缺血再灌注大鼠脑组织具有保护作用。
Objective: To investigate the effects of salvianolic acid B(Sal B) on cerebral injury,angiogenesis and oxidative stress in rats with focal cerebral ischemia reperfusion,and its protective effect on brain injury. Methods :40 SD rats were divided into four groups:healthy rats group (Ctrl);Drug group:healthy rats were injected with Sal B 50 mg/kg Body weight;Model group:the model of focal cerebral ischemia reperfusion(MCAO) was established based on the reference literature;Model addition group (MCAO+Sal B):Sal B 50 mg/kg BW was injected intraperitoneally into rats 3 d before modeling,once a day,2 h after reperfusion.The rats in each group were sacrificed 24 h after modeling.Hematoxylin and eosin(HE)staining was used to detect the pathological damage of brain tissue in rats.Apoptosis of brain tissue cells was detected by TUNEL staining.The concentration of Malonaldehyde(MDA),Superoxide dismutase (SOD) and Lactate dehydrogenase (LDH) were determined by assay kits.The expression of Intercellular adhesion molecule 1(ICAM-1) was detected by Immunohistochemical.The expression of Vascular endothelial growth factor(VEGF) and its receptor VEGFR2,P38 and Hsp27 phosphorylation level were detected by Western blot. Results: Compared with the control group, there was obvious tissue lesion in the brain tissue of the model group.The apoptotic cell ratio was significantly increased ( P <0.01).The content of SOD decreased obviously, and the content of MDA and LDH increased obviously ( P < 0.01).The expression of ICAM-1 was significantly up-regulated ( P < 0.01).The expression of VEGF and VEGFR2 was significantly up-regulated ( P <0.01).Phosphorylation levels of P38 and Hsp27 were significantly increased ( P <0.01).Compared with the model group, the brain tissue pathological damage of rats in medicine treatment groups was significantly alleviated,and apoptotic cells were significantly reduced ( P <0.01).SOD content was significantly increased, MDA and LDH content were significantly decreased ( P <0.01).The protein expression ICAM-1 wa
作者
吕娟
赵红梅
孙桂芳
王润青
LU Juan;ZHAO Hong-Mei;SUN Gui-Fang;WANG Run-Qing(Department of Neurology,Zhengzhou Central Hospital, Zhengzhou 450000,China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2019年第10期1174-1178,共5页
Chinese Journal of Immunology
基金
河南省科技厅基金资助项目(201230989409K)资助
关键词
丹酚酸B
脑缺血再灌注
血管新生
氧化应激
Salvianolic acid B
Cerebral ischemiareperfusion
Angiogenesis
Oxidative stress
