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目的探讨川芎嗪对失神经骨骼肌细胞凋亡及bcl-2、bax表达的影响,寻找延缓失神经骨骼肌萎缩的新途径。方法将54只Wistar大鼠,随机分为9组,分别为正常对照组(A)、失神经对照组(B、C、D、E)、川芎嗪干预组(F、G、H、I)。失神经对照组、川芎嗪干预组建立右下肢失神经腓肠肌动物模型。正常对照组(0d)不做任何处理;川芎嗪干预组于腹腔注射川芎嗪注射液80mg.kg-1.d-1;失神经对照组腹腔注射等剂量生理盐水。在术后第0、2、7、14、28d分别处死1组大鼠取其两侧腓肠肌并称肌湿重。采用RT-PCR、Western Blot检测各时段bcl-2以及bax的蛋白表达水平。使用TUNEL法检测肌细胞凋亡。结果川芎嗪干预组肌湿质量比显著高于失神经对照组(P<0.05)。川芎嗪干预组bcl-2的蛋白表达水平均高于失神经对照组(P<0.05),而bax的蛋白表达水平均低于失神经对照组(P<0.05)。失神经组凋亡率逐渐升高,且与正常对照组相比差异有统计学意义(P<0.05),采用川芎嗪治疗2d时,细胞凋亡率显著低于同期失神经对照组(P<0.05)。结论川芎嗪可以通过促进bcl-2抑制bax的表达来延缓失神经骨骼肌萎缩。
Objective To investigate the effects of ligustrazine on the apoptosis and the expression of bcl-2 and bax in skeletal muscle cells of denervated nerve and to find a new way to delay the atrophy of denervated skeletal muscle. Methods Fifty - four Wistar rats were randomly divided into 9 groups: normal control group (A), denervated control group (B, C, D, E), ligustrazine intervention group (F, G, H, . Rats in denervation group and ligustrazine group were established animal models of denervated gastrocnemius in the right lower extremity. Normal control group (0d) without any treatment; Ligustrazine intervention group intraperitoneal injection of ligustrazine injection 80mg.kg-1.d-1; no nerve control group intraperitoneally injected with normal saline. At 0, 2, 7, 14, and 28 days after operation, 1 group of rats were sacrificed and their gastrocnemius muscles were harvested. RT-PCR and Western Blot were used to detect the protein expression of bcl-2 and bax at each time point. Myocyte apoptosis was detected by TUNEL method. Results The muscle mass ratio in the ligustrazine group was significantly higher than that in the control group (P <0.05). The protein expression of bcl-2 in the LPS group was higher than that in the denervated group (P <0.05), while the protein expression of bax was lower than that of the denervated group (P <0.05). The apoptotic rate of the denervated group gradually increased, and the difference was statistically significant compared with the normal control group (P <0.05). When treated with tetramethylpyrazine for 2 days, the apoptotic rate was significantly lower than that of the denervated group (P < 0.05). Conclusion Tetramethylpyrazine can delay denervated skeletal muscle atrophy by inhibiting the expression of bax by bcl-2.