摘要
目的研究胡黄连苷Ⅱ对大鼠脑缺血再灌注损伤后的抗氧化作用和可能的机制。方法采用线栓法对90只成年健康雄性、vistar大鼠建立大鼠大脑中动脉闭塞再灌注（MCA0／R）模型。按随机数字表法分组，治疗组和阳性对照组分别经尾静脉注射胡黄连苷Ⅱ（10m/kg）和丹参素钠（10mg/kg），阴性对照组和假手术组给予0．1mol／L PBS 250μl。Bederson评分法评价动物的神经行为功能，氯化三苯基四氮唑染色检测脑梗死体积，TUNEL法检测神经细胞凋亡，免疫组织化学法检测诱导性-氧化氮合酶（iNOS）和超氧化物歧化酶（SOD）的表达，酶联免疫吸附试验检测脑组织中iNOS和SOD蛋白的浓度。结果脑缺血再灌注损伤后，大鼠均表现神经功能障碍、行为异常，缺血侧出现脑梗塞病灶，神经细胞凋亡数量增多，iNOs表达增强，SOD表达减弱。治疗组治疗后，动物神经行为功能损伤程度明显改善[（1．28±0．38）]分、脑梗塞体积缩小[（68．73±4．46）％]、凋亡神经细胞数明显减少[（6．10±1．26）细胞数／视野]、iNOS表达降低（4．67±0．51）、SOD表达增强（O．53±0．14），与阴性对照组比较差异有统计学意义0值分别为3．16、2．5l、4．15、3．12、3．25，P均〈0．05）。结论脑缺血再灌注损伤后，胡黄连苷Ⅱ可能通过抑制细胞凋亡和调节iNOS、SOD的表达发挥神经保护作用。
Objective To investigate the anti-oxidant effect and the possible mechanisms ofpicrodideII in cerebral ischemia/reperfusion injuries in rats. Methods A total of 90 adult, healthy, male Wistar rats were used to established the middle cerebral artery occlusion reperfusion （MCAO/R） models by intraluminal monofilament suture on the left external-internal carotid artery. The treatment group and the positive control group were respectively injected with 1.0% picroside II （10 mg/kg, 250 μl） and salvianic acid A sodium （10 mg/kg, 250 μl） via the tail vein, and the negative control group and sham-surgery group were injected with 0.1 mol/L phosphate buffer saline （PBS） 250 μl. The neurological deficit scores were evaluated with Bederson＇s test. The cerebral infarction volume was observed with tetrazolium （TTC） staining. The apoptosis positive cells were counted by terminal deoxynucleotidyl transferase dUTP nick-end labeling and the expressions of inducible nitric oxide synthase （iNOS） and superoxide dismutase （SOD） were detected with immunohistochemical assay. The concentration of iNOS and SOD proteins in brain tissue was detected by enzyme linked immunosorbent assay. Results Neurological behavioral malfunction appeared in all the rats with MCAO/R. The infarction focuses emerged in the ischemic hemisphere following the MCAO/R injuries. The number of apoptotic cells and the expression of iNOS increased while the SOD reduced after MCAO/R. After the treatment ofpicrodideⅡ, the nervous behavioral function （1.28± 0.38）improved, the infarction volume （68.73±4.46） % reduced, the number of apoptosis positive cells （6.10± 1.26）, the expressions and the concentrations in brain tissue of iNOS （4.67±0.51） decreased while those of SOD （0.53 ± 0.14） increased significantly compared with the negative control groups （t = 3.16, 2.51, 4.15, 3.12, 3.25, P〈0.05）. Conclusion Picrodide Ⅱ might play a neuroprotective effect by inhibiting the neuronal apoptosis and the expressions ofiNOS and SOD after cerebral ischemia/reperfusion injuries.
出处
《国际中医中药杂志》
2011年第9期803-806,共4页
International Journal of Traditional Chinese Medicine
关键词
胡黄连苷-Ⅱ
丹参素钠
脑缺血
再灌注损伤
Picroside Ⅱ
Salvianic acid A sodium
Cerebral ischemia
Reperfusion injury
