髓复康对脑缺血大鼠缺血损伤区硫酸软骨素蛋白多糖及生长相关蛋白43表达的影响

Effect of Suifukang on the Expression of Chondroitin Sulfate Proteoglycans and Axonal Growth Promoting Factors in Ischemic Brain Region of Cerebral Ischemic Rats

目的观察髓复康对脑缺血大鼠脑缺血损伤的修复作用机制。方法将144只大鼠随机分为正常组、模型组、阳性对照组和髓复康大、中、小剂量组,每组24只,除正常组外其余各组大鼠建立右侧大脑中动脉阻塞(MCAO)再灌注模型,髓复康大、中、小剂量组分别灌胃髓复康浓缩剂5g/100g、2.5g/100g、1.25g/100g,每日1次;阳性对照组腹腔注射甲基强地松龙30mg/kg,隔日1次;模型组灌胃等量生理盐水,正常组不做任何处理。各组在给药8、15和30天取大鼠脑组织,免疫组织化学方法检测各组大鼠脑缺血损伤区硫酸软骨素蛋白多糖(CSPGs)、生长相关蛋白43(GAP-43)表达量。结果各组给药8、15和30天时组内比较,CSPGs及GAP-43表达差异无统计学意义(P>0.05)。各时间点与正常组比较,模型组CSPGs表达显著增强(P<0.01);各给药组CSPGs表达显著低于模型组(P<0.05或P<0.01)。各时间点与正常组比较,模型组GAP-43表达差异无统计学意义(P>0.05);与模型组比较,髓复康大、中、小剂量组GAP-43表达显著增强(P<0.05或P<0.01)。结论髓复康可以抑制大鼠脑缺血损伤区CSPGs的表达,促进GAP-43的表达,可能通过改善脑缺血损伤区轴突再生的微环境,从而促进脑缺血损伤后轴突的再生。

Objective To study the effect and mechanism of Suifukang （brain-marrow rehabilitation formula） on cerebral ischemic injury in rats. Methods Totally 144 rats were randomized into the normal group, model group, positive control group and Suifukang large-dose, middle-dose and small-dose groups, with 24 in each. The right middle cerebral artery occlusion （MCAO） and reperfusion rat models were established in each group except the normal group. The rats in Suifukang large-dose, middle-dose and small-dose groups were gavaged with 5 g, 2.5 g and 1.25 g crude drug of Suifukang per 100 g once daily. The positive control group was given intraperitoneal injection of 30mg/kg methylprednisolone every other day. The model group was gavaged with the same amount of normal saline and the normal group received no treatment. The brain tissues were removed in each group on the 15th and 30th day of administration. The expression of chondroitin sulfate proteoglycans （CSPGs）and growth associated protein 43 （GAP-43）CSPGs and GAP-43 in ischemic brain region of rats in each group was detected by immunohistoehemistry method. Results In-group comparisons showed that there was no significant difference in the expression of GSPGs and GAP-43 on the 8th, 15th and 30th day of administration （P〉0.05）. Comparing with the normal group, the expression of GSPGs was significantly increased in the model group （P〈0.01）. Comparing with the model group, the expression of GSPGs in the administration groups were significantly decreased （P〈0.05 or P〈0.01）. There was no significant difference in the expression of GAP-43 between the normal group and model group （P〉0.05）. Comparing with the model group, the expression, of GAP-43 in the Suifukang large-dose, middle-dose and small-dose groups was significantly increased （P〈0.05 or P〈0.01）. Conclusion Suifukang can inhibit the expression of GSPGs and promote the expression of GAP-43 in ischemic brain region of rats, which may be related to improving the microenvironment of axonal regeneration in ischemic brain region and promoting axonal regeneration after cerebral isehemia.