国际免疫学杂志
國際免疫學雜誌
국제면역학잡지
INTERNATIONAL JOURNAL OF IMMUNOLOGY
2008年
5期
324-326,393
,共4页
宫凌涛%李继红%石学魁%王亚贤
宮凌濤%李繼紅%石學魁%王亞賢
궁릉도%리계홍%석학괴%왕아현
脑梗塞%中药活脑康%TGF-β1%P38
腦梗塞%中藥活腦康%TGF-β1%P38
뇌경새%중약활뇌강%TGF-β1%P38
Cerbral infarction%Traditional Chinese medicine HUONAOKANG%TGF-β1%P38
目的 观察中药活脑康对脑缺血大鼠脑组织中TGF-β1和突触素P38表达的影响.方法 用线栓法制备大鼠局灶性脑缺血模型;应用SABC免疫组化染色法观察脑组织中TGF-β1和P38的表达.结果 TGF-β1和P38在正常脑神经细胞中均呈弱阳性表达,脑缺血后,TGF-β1和P38的表达量均明显增强(与正常对照组相比P<0.01,有统计学意义);中药活脑康对缺血脑组织中TGF-β1和P38的表达有上调作用(与模型组相比分别为P<0.01和P<0.001,有统计学意义).结论 中药活脑康可能是通过增加TGF-β1和P38的表达减少脑细胞的凋亡,促进突触再建,增强和完善再建突触效能发挥脑保护作用.
目的 觀察中藥活腦康對腦缺血大鼠腦組織中TGF-β1和突觸素P38錶達的影響.方法 用線栓法製備大鼠跼竈性腦缺血模型;應用SABC免疫組化染色法觀察腦組織中TGF-β1和P38的錶達.結果 TGF-β1和P38在正常腦神經細胞中均呈弱暘性錶達,腦缺血後,TGF-β1和P38的錶達量均明顯增彊(與正常對照組相比P<0.01,有統計學意義);中藥活腦康對缺血腦組織中TGF-β1和P38的錶達有上調作用(與模型組相比分彆為P<0.01和P<0.001,有統計學意義).結論 中藥活腦康可能是通過增加TGF-β1和P38的錶達減少腦細胞的凋亡,促進突觸再建,增彊和完善再建突觸效能髮揮腦保護作用.
목적 관찰중약활뇌강대뇌결혈대서뇌조직중TGF-β1화돌촉소P38표체적영향.방법 용선전법제비대서국조성뇌결혈모형;응용SABC면역조화염색법관찰뇌조직중TGF-β1화P38적표체.결과 TGF-β1화P38재정상뇌신경세포중균정약양성표체,뇌결혈후,TGF-β1화P38적표체량균명현증강(여정상대조조상비P<0.01,유통계학의의);중약활뇌강대결혈뇌조직중TGF-β1화P38적표체유상조작용(여모형조상비분별위P<0.01화P<0.001,유통계학의의).결론 중약활뇌강가능시통과증가TGF-β1화P38적표체감소뇌세포적조망,촉진돌촉재건,증강화완선재건돌촉효능발휘뇌보호작용.
Objective To observe the effects of traditional Chinese medicine HUONAOKANG on the expressionof TGF-β1 and P38 of rats with cerebral ischemic injury. Methods Focal cerebral ischemic model of cerebralmiddle artery occlusion was duplicated with nylon thread. The expression of TGF-β1 and P38 were determinedby SABC immunohistochemical method. Results No significant TGF-β1 and P38 expression was detected incontrol group. After cerebral ischemic injury, the expression of TGF-β1 and P38 were increased (comparedwith control group, P <0.01 ). HUONAOKANG increased the expression TGF-β1 and P38 obviously ( Com-pared with ischemic group, P < 0.01 and P < 0. 001, respectively). Conclusion HUONAOKANG signifi-cantly , increased the expression of TGF-β1 and P38, which might be the mechanism of protecting ischemic in-jury of brain tissue.