中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2014年
6期
571-575
,共5页
甄雪克%梁剑峰%杨文强%邵旭%张黎%于炎冰
甄雪剋%樑劍峰%楊文彊%邵旭%張黎%于炎冰
견설극%량검봉%양문강%소욱%장려%우염빙
丹红注射液%雪旺细胞%脑源性神经因子
丹紅註射液%雪旺細胞%腦源性神經因子
단홍주사액%설왕세포%뇌원성신경인자
Danhong injection%Schwann cell%Brain-derived neurotrophic factor
目的 探讨丹红注射液(DH)对SD大鼠雪旺细胞(SC)表达脑源性神经因子(BDNF)的促进作用及其机制. 方法 在测定DH对糖基化终末产物(AGEs)导致的SC凋亡的影响实验中将SC分成对照组、SC+AGEs组、SC+DH+AGEs组,培养48 h后对同倍视野下SC细胞计数并比较;在测定DH对SC BDNF mRNA和蛋白的表达影响实验中,运用实时定量逆转录聚合酶链反应(RT-PCR)和Western blotting技术检测BDNF mRNA和蛋白;在测定DH在不同抑制剂作用下对BDNF mRNA表达的影响实验中,运用RT-PCR技术对BDNFmRNA进行检测. 结果 (1)AGEs+SC组SC数量较对照组明显减少,SC+DH+AGEs组较AGEs+SC组SC数量明显增加,差异有统计学意义(P<0.05);(2)DH+SC组BDNF mRNA和蛋白较对照组均明显增高,差异有统计学意义(P<0.05);(3)与对照组相比,DH+Calphostin C(蛋白激酶C抑制剂)组BDNF mRNA表达量明显减少,差异有统计学意义(P<0.05);(4)与对照组相比,DH+U0126(甲乙基酮抑制剂)、DH+FR 180204(细胞外调节蛋白激酶)、DH+SB203580(p38蛋白抑制剂)3组BDNF mRNA的表达量均明显降低,差异有统计学意义(P<0.05). 结论 (1)DH可明显抑制AGEs导致的SC的凋亡;(2)DH可促进SC BDNF mRNA和蛋白的表达;(3)蛋白激酶C及下游的甲乙基酮、细胞外调节蛋白激酶和p38蛋白通路可能参与了DH对BDNF mRNA表达的上调作用.
目的 探討丹紅註射液(DH)對SD大鼠雪旺細胞(SC)錶達腦源性神經因子(BDNF)的促進作用及其機製. 方法 在測定DH對糖基化終末產物(AGEs)導緻的SC凋亡的影響實驗中將SC分成對照組、SC+AGEs組、SC+DH+AGEs組,培養48 h後對同倍視野下SC細胞計數併比較;在測定DH對SC BDNF mRNA和蛋白的錶達影響實驗中,運用實時定量逆轉錄聚閤酶鏈反應(RT-PCR)和Western blotting技術檢測BDNF mRNA和蛋白;在測定DH在不同抑製劑作用下對BDNF mRNA錶達的影響實驗中,運用RT-PCR技術對BDNFmRNA進行檢測. 結果 (1)AGEs+SC組SC數量較對照組明顯減少,SC+DH+AGEs組較AGEs+SC組SC數量明顯增加,差異有統計學意義(P<0.05);(2)DH+SC組BDNF mRNA和蛋白較對照組均明顯增高,差異有統計學意義(P<0.05);(3)與對照組相比,DH+Calphostin C(蛋白激酶C抑製劑)組BDNF mRNA錶達量明顯減少,差異有統計學意義(P<0.05);(4)與對照組相比,DH+U0126(甲乙基酮抑製劑)、DH+FR 180204(細胞外調節蛋白激酶)、DH+SB203580(p38蛋白抑製劑)3組BDNF mRNA的錶達量均明顯降低,差異有統計學意義(P<0.05). 結論 (1)DH可明顯抑製AGEs導緻的SC的凋亡;(2)DH可促進SC BDNF mRNA和蛋白的錶達;(3)蛋白激酶C及下遊的甲乙基酮、細胞外調節蛋白激酶和p38蛋白通路可能參與瞭DH對BDNF mRNA錶達的上調作用.
목적 탐토단홍주사액(DH)대SD대서설왕세포(SC)표체뇌원성신경인자(BDNF)적촉진작용급기궤제. 방법 재측정DH대당기화종말산물(AGEs)도치적SC조망적영향실험중장SC분성대조조、SC+AGEs조、SC+DH+AGEs조,배양48 h후대동배시야하SC세포계수병비교;재측정DH대SC BDNF mRNA화단백적표체영향실험중,운용실시정량역전록취합매련반응(RT-PCR)화Western blotting기술검측BDNF mRNA화단백;재측정DH재불동억제제작용하대BDNF mRNA표체적영향실험중,운용RT-PCR기술대BDNFmRNA진행검측. 결과 (1)AGEs+SC조SC수량교대조조명현감소,SC+DH+AGEs조교AGEs+SC조SC수량명현증가,차이유통계학의의(P<0.05);(2)DH+SC조BDNF mRNA화단백교대조조균명현증고,차이유통계학의의(P<0.05);(3)여대조조상비,DH+Calphostin C(단백격매C억제제)조BDNF mRNA표체량명현감소,차이유통계학의의(P<0.05);(4)여대조조상비,DH+U0126(갑을기동억제제)、DH+FR 180204(세포외조절단백격매)、DH+SB203580(p38단백억제제)3조BDNF mRNA적표체량균명현강저,차이유통계학의의(P<0.05). 결론 (1)DH가명현억제AGEs도치적SC적조망;(2)DH가촉진SC BDNF mRNA화단백적표체;(3)단백격매C급하유적갑을기동、세포외조절단백격매화p38단백통로가능삼여료DH대BDNF mRNA표체적상조작용.
Objective To investigate the promotion effect of Danhong injection (DH) on brain-derived neurotrophic factor (BDNF) expression in Schwann cells (SCs) of SD rats.Methods In experiment of SCs apoptosis induced by advanced glycation end products (AGEs),SCs were divided into control group,AGEs treatment group and DH+AGEs treatment group; 48 h after each treatment,the SCs count was compared.In experiment of DH affecting mRNA and protein BDNF expressions in SCs,real time-PCR and Western blotting were used.In the experiment of DH combined with different inhibitors (Calphostin C,LY294002,H89,U0126,FR180204 and SB203580) affecting mRNA BDNF expression in SCs,real time-PCR was used.Results The number of SCs in AGEs treatment group was significantly decreased than that in the control group,but that in DH+AGEs treatment group was statistically increased than that in AGEs group (P<0.05).The mRNA and protein expressions of BDNF in the DH treatment group were significantly increased than those in the control group (P<0.05).As compared with DH group,DH+Calphostin C treatment group had significantly decreased BDNF mRNA expression (P<0.05); BDNF mRNA expression in the DH+U0126,DH+FR180204 and DH+SB203580 treatment groups was significantly decreased as compared with that in the DH treatment group (P<0.05).Conclusions DH could effectively inhibit SCs apoptosis induced by AGEs and significantly promote BDNF expression;protein kinase C (Calphostin C) and mehtyl ethyl ketone (U0126)/extracellular regulated protein kinases (FR180204EK)/p38 (SB203580) may be the important signaling transconduction pathways for BDNF expression.