电针对吗啡戒断大鼠胸腺细胞凋亡相关基因的影响

目的:探讨电针抗吗啡戒断大鼠胸腺细胞凋亡的作用机制。方法:40只SD大鼠随机分为正常组、对照组、依赖组、电针组,连续20d递增量肌肉注射吗啡造成吗啡成瘾模型。造模后,依赖组立刻处死;对照组观察7d后处死;电针组电针双侧"足三里"穴(2/100Hz,2~4mA),每日1次,每次30min,治疗7d后处死。取大鼠胸腺,用免疫组化法检测凋亡基因Bcl-2、Bax、Fas、FasL蛋白表达。结果:与正常组比较,对照组和依赖组Bcl-2表达明显减少,Bax明显增加(P<0.01);电针组与对照组相比,Bcl-2表达上升(P<0.05),Bax表达的下降尚未达到统计学意义(P>0.05)。对照组及依赖组Fas、FasL的表达比正常组明显升高(P<0.01);电针组与对照组相比,Fas、FasL的表达均明显减少,差异显著(P<0.01)。结论:电针"足三里"穴增加吗啡戒断大鼠胸腺细胞内Bcl-2蛋白表达的水平,减少Bax蛋白表达水平,降低Bax/Bcl-2比值,抑制Fas、FasL表达水平的提高,可能是电针抗吗啡戒断大鼠胸腺细胞凋亡的作用机制之一。

Effect of Electroacupuncture on Thymocyte Apoptosis-related Genes in Morphine Withdrawal Rats

OBJECTIVE: To explore the underlying mechanism of electroacupuncture (EA) in relieving morphine withdrawal syndrome in rats. METHODS: Forty SD rats were randomly divided into normal control group, model group 1, model group 2 and EA group. Morphine withdrawal syndrome model was established by muscular injection of morphine (5 mg/kg on the 1st day, progressively increasing everyday till 100 mg/kg on the 20th day) in the hind limbs. Then, rats of model group 1 were anesthetized (10% chloraldurat) to be killed on the 21st day, and those of model group 2 killed on the 27th day. EA (2/100 Hz, 2-4 mA) was applied to bilateral "Zusanli" (ST 36) for 30 mm, once a day for 7 days. The rat's thymus was removed (after anesthesia), cut into sections (4 pm) and stained with immunohistochemical method for displaying the expression of apoptotic promoters Bax, Fas, Fas Ligand (FasL) as well as anti-apoptotic peptide Bcl-2. RESULTS: Compared with normal group, Bcl-2 immunoreaction (IR)-positive cell number of model group 1 and group 2 decreased significantly while Sax, Fas and FasLIR-positive cell number and Bax/Bcl-2 in two model groups increased considerably (P < 0.01). In comparison with model group 2, Bcl-2 IR-positive cell number of model group 1 decreased significantly (P < 0.05), Bax, Fas and FasL IR-positive cell number and Bax/Bcl-2 of model group 1 were significantly higher (P < 0.01, fl. 05). After EA, in comparison with model group 2, Fas and FasL IR-positive cell number and Bax/Bcl-2 decreased significantly (P < 0.01, 0.05), and Bcl-2 IR-positive cell number increased markedly in EA group (P < 0.05); in comparison with model group 1, Bcl-2 IR-positive cell number increased significantly (P < 0.01), while Bax, Fas and FasL IR-positive cell number and Bax/Bcl-2 decreased evidently in EA group (P < 0.01). CONCLUSION: EA at "Zusanli" (ST 36) can inhibit morphine-induced downregulation of Bcl-2 and upregulation of Fas and FasL expression, which may contribute to its effect in resisting thymus apoptosis in morphine withdrawal rats.