中国医药
中國醫藥
중국의약
CHINA MEDICINE
2010年
7期
613-615
,共3页
脑梗死%通咽止呃方%凋亡基因%大鼠
腦梗死%通嚥止呃方%凋亡基因%大鼠
뇌경사%통인지애방%조망기인%대서
Focal cerebral infarction%Tongyanzhi'e prescription%Apoptosis genes%Rat
目的 探讨通咽止呃方对局灶性脑梗死大鼠脑组织损伤的影响及其可能的机制.方法 48例雄性Wistar大鼠完全随机分为假手术组,模型组,通咽止呃方低、中、高剂量组及尼莫地平组,每组8只.除假手术组外各组均予手术造模,造模前7d灌胃给药.检测各组大鼠脑组织细胞凋亡基因(Bcl-2)和细胞凋亡促进基因(Bax)的表达情况.结果 假手术组,模型组,通咽止呃组方低、中、高剂量组,尼莫地平组大鼠Bax及Bcl-2水平分别为[(2.175±0.311)ng/L、(1.950±0.245)ng/L,(9.175±0.320)ng/L、(5.737±0.297)ng/L,(8.913±0.331)ng/L、(5.763±0.354)ng/L,(8.050±0.288)ng/L、(5.987±0.331)ng/L,(6.913±0.348)ng/L、(6.913±0.402)ng/L,(7.025±0.230)ng/L、(7.125±0.406)ng/L].与假手术组相比,其他各组大鼠脑内Bax、Bcl-2表达明显较高(P＜0.01);与模型组相比,通咽止呃方中、高剂量组及尼莫地平组大鼠脑组织内Bax表达明显偏低(P＜0.01).Bcl-2在通咽止呃方高剂量及尼莫地平组大鼠脑组织内明显较高(P＜0.01).结论 通咽止呃方对局灶性脑梗死大鼠脑组织损伤具有保护作用,可能与促进缺血性脑损害时细胞凋亡过程终止并逆转等机制有关.
目的 探討通嚥止呃方對跼竈性腦梗死大鼠腦組織損傷的影響及其可能的機製.方法 48例雄性Wistar大鼠完全隨機分為假手術組,模型組,通嚥止呃方低、中、高劑量組及尼莫地平組,每組8隻.除假手術組外各組均予手術造模,造模前7d灌胃給藥.檢測各組大鼠腦組織細胞凋亡基因(Bcl-2)和細胞凋亡促進基因(Bax)的錶達情況.結果 假手術組,模型組,通嚥止呃組方低、中、高劑量組,尼莫地平組大鼠Bax及Bcl-2水平分彆為[(2.175±0.311)ng/L、(1.950±0.245)ng/L,(9.175±0.320)ng/L、(5.737±0.297)ng/L,(8.913±0.331)ng/L、(5.763±0.354)ng/L,(8.050±0.288)ng/L、(5.987±0.331)ng/L,(6.913±0.348)ng/L、(6.913±0.402)ng/L,(7.025±0.230)ng/L、(7.125±0.406)ng/L].與假手術組相比,其他各組大鼠腦內Bax、Bcl-2錶達明顯較高(P＜0.01);與模型組相比,通嚥止呃方中、高劑量組及尼莫地平組大鼠腦組織內Bax錶達明顯偏低(P＜0.01).Bcl-2在通嚥止呃方高劑量及尼莫地平組大鼠腦組織內明顯較高(P＜0.01).結論 通嚥止呃方對跼竈性腦梗死大鼠腦組織損傷具有保護作用,可能與促進缺血性腦損害時細胞凋亡過程終止併逆轉等機製有關.
목적 탐토통인지애방대국조성뇌경사대서뇌조직손상적영향급기가능적궤제.방법 48례웅성Wistar대서완전수궤분위가수술조,모형조,통인지애방저、중、고제량조급니막지평조,매조8지.제가수술조외각조균여수술조모,조모전7d관위급약.검측각조대서뇌조직세포조망기인(Bcl-2)화세포조망촉진기인(Bax)적표체정황.결과 가수술조,모형조,통인지애조방저、중、고제량조,니막지평조대서Bax급Bcl-2수평분별위[(2.175±0.311)ng/L、(1.950±0.245)ng/L,(9.175±0.320)ng/L、(5.737±0.297)ng/L,(8.913±0.331)ng/L、(5.763±0.354)ng/L,(8.050±0.288)ng/L、(5.987±0.331)ng/L,(6.913±0.348)ng/L、(6.913±0.402)ng/L,(7.025±0.230)ng/L、(7.125±0.406)ng/L].여가수술조상비,기타각조대서뇌내Bax、Bcl-2표체명현교고(P＜0.01);여모형조상비,통인지애방중、고제량조급니막지평조대서뇌조직내Bax표체명현편저(P＜0.01).Bcl-2재통인지애방고제량급니막지평조대서뇌조직내명현교고(P＜0.01).결론 통인지애방대국조성뇌경사대서뇌조직손상구유보호작용,가능여촉진결혈성뇌손해시세포조망과정종지병역전등궤제유관.
Objective To approach the effect and possible mechanism of Tongyanzhie prescription on rat focal cerebral infarct injury. Methods Totally 48 cases of male Wistar rats were randomly divided into sham-operation group, model group, Tongyanzhie prescription low, medium, and high dose group and Nimodipine group. Operative model was made in each group except sham-operation group. Drugs were given 7 days before operation. The expression of Bcl-2 and Bax was evaluated. Results The levels of Bcl-2 and Bax in the six groups were (2. 175 ±0.311)ng/L and (1.950 ±0.245)ag/L,(9.175 ±0.320)ng/L and (5.737 ±0.297)ag/L, (8.913 ±0.331)ng/L and (5.763 ± 0.354 ) ng/L, ( 8.050 ± 0.288 ) ng/L and (5.987 ± 0.331) ng/L, ( 6.913 ± 0.348) ng/L and(6.913 ± 0.402 ) ng/L, (7.025 ± 0.230 ) ng/L and ( 7.125 ± 0.406 ) ng/L, respectively. Compared with sham-operation group, other five groups showed a higher expression of Bcl-2 and Bax( P ＜0. 01 ). Compared with the model group, the expression of Bax of other four groups expressed significantly lower( P ＜ 0.01 ). The Bcl-2 level was obviously higher in the high dose group and Nimodipine group. Conclusions Tongyanzhie prescription alleviates the focal cerebral infarction injury in rats. The possible mechanism may be related to the termination and reversion of neuron apoptosis in ischemic cerebral injury.
