Objective To investigate the protective effects and its possible mechanisms of Hua Yu Ke Sai capsule pre-treatment on the brain after ischemia injury in rats. Methods 40 rats were randomely divided into A, B, C and D group. Rats in C, D groups were treated by Hua Yu Ke Sai capsule( 12. 2, 24.4 g/kg) 7 days before MCAO, 2/day; whereas A, B groups were given NS. 6 hours after ischemia, rats in each group were used to estimate the neurological deficit score and determination of ET and NO. Results The neurological deficit score of A, B, C and D group was 0,3.07 ±0.73, 1.96 ± 0.64, 1.22 ±0.67; the expression of NO was (58.03 ±5. 09), (36. 98 ±9. 66), (47. 52 ±7. 88), (51. 87 ± 7. 34) μmol/L; the expression of ET was (215.75 ±23. 34) ,(326. 28 ±35. 5), (244. 85 ± 17. 55) ,(227.15 ±23. 69)pg/ml. The differences among A, B, C, D group were significantly remarkable(all P <0. 05). Conclusion Hua Yu Ke Sai capsule can protect the brain from ischemia injury, and the neuro protections mechenism may be related to the decrease of ET and the increase of NO.%目的 观察化瘀克塞胶囊预处理对局灶性脑缺血大鼠神经功能的影响,并探讨其可能的机制.方法 将40只Wistar大鼠随机分为A、B、C、D组,造模前7d开始灌胃.C、D组给予化瘀克塞胶囊12.2、24.4 g/kg,2次/d;A、B组则给予等体积的生理盐水.B、C、D组采用线栓法制备大脑中动脉缺血模型,A组只显露大脑中动脉但不栓塞.持续性缺血6h后,行大鼠行神经功能缺损评分,检测血浆中的内皮素(ET)、一氧化氮(N0).结果 A、B、C、D组神经功能缺损评分分别为0、(3.07±0.73)、(1.96±0.64)、(1.22±0.67)分,血浆NO水平分别为(58.03±5.09)、(36.98±9.66)、(47.52±7.88)、(51.87±7.34) μmol/L,血浆ET水平分别为(215.75±23.34)、(326.28±35.5)、(244.85±17.55)、(227.15±23.69) pg/ml;各组间两两比较,P均<0.05.结论 化瘀克塞胶囊可通过提高局灶性脑缺血大鼠血浆NO水平、减少血浆ET的释放,促进神经功能能恢复.
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