中文摘要：

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48h后对同倍视野下SC细胞计数并比较：在测定DH对SCBDNFmRNA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BDNF mRNA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BDNFmRNA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＋CalohostinC（蛋白激酶C抑制剂）组BDNFmRNA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＋FR180204（细胞外调节蛋白激酶1、DH＋SB203580（p38蛋白抑制剂）3组BDNFmRNA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SCBDNFmRNA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BDNFmRNA表达的上调作用。

英文摘要：

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.