复方中药丹星通络汤对大鼠局灶性脑缺血再灌注损伤的保护作用

目的:探讨复方中药丹星通络汤对大鼠局灶性脑缺血再灌注脑损伤的保护作用及机制. 方法:40只大鼠随机分为4组,即对照组(假手术 生理盐水)、模型组(缺血再灌注 生理盐水)、尼莫地平组(缺血再灌注 尼莫地平)、复方丹星通络汤组(缺血再灌注 复方丹星通络汤). 每组分别连续5 d灌胃口服生理盐水、尼莫地平、复方丹星通络汤. 线栓法制作局灶性脑缺血再灌注模型,缺血2 h后再灌注24 h. 检测血清乳酸脱氢酶(LDH)活力、大脑FAS细胞表达. 结果:模型组大鼠局灶性脑缺血再灌注后血清LDH活力明显高于对照组(P＜0.05), 尼莫地平组、复方丹星通络汤组血清中LDH活力明显降低(尼莫地平组vs 模型组,P＜0.01; 复方丹星通络汤组vs模型组,P＜0.05),尼莫地平组和复方丹星通络汤组间无显著性差异(P＞0.05). 模型组大脑FAS细胞表达明显高于对照,尼莫地平,复方丹星通络汤组(P＜0.01),与模型组比较,尼莫地平组、复方丹星通络汤组脑组织FAS阳性细胞数表达显著下调(P＜0.01),复方丹星通络汤组明显低于尼莫地平组(P＜0.01). 结论:复方丹星通络汤可有效地防止FAS及LDH升高, 对脑缺血再灌注脑损伤有显著保护作用.

Neuroprotective effect of DanXingTongLuoTang on rats with focal cerebral ischemia-reperfusion injury

AIM: To study the neuroprotection and mechanism of danxingtongluotang (DX) on rats with focal cerebral ischemia-reperfusion (I/R) injury. METHODS: Forty SD male rats were divided randomly into 4 groups: control group, sham-operated + normal saline (NS); model group, cerebral I/R+NS; nimodi- pine group, I/R+nimodipine; DX group, I/R+DX. The 4 groups were fed with NS, nimodipine or DX for consecutive 5 d. Focal I/R models were made with suture-occlusion method. After cerebral ischemia for 2 h and then reperfusion for 24 h, the acti- vity of LDH in serum was measured and the expression of FAS in brain tissue was detected. RESULTS: After cerebral I/R, the activity of LDH in serum of model group increased significantly as compared with control group (P<0.05); the activity of LDH in nimodipine group and DX group decreased obviously and was lower than that in model group (P<0.05, P<0.01), there was no significant difference between the activity of nimodipine group and DX group (P>0.05). Expression of FAS in brain tissue of model group increased significantly as compared with that in control, nimodipine and DX groups (P<0.01); the expression of FAS in brain tissue of nimodipine and DX groups was decreased significantly as compared with that in model group(P<0.01); the level of DX group was lower than that of nimodipine group. CONCLUSION: DX has an obvious protection against I/R injury probably through decreasing the activity of LDH and the expression of FAS in brain tissue.