Song Xiao-ge, Zhu Yong-lei, Zhang Rong-jun, Zhang Yao, Liu Xian-hua
Institute of Acu-moxibustion, An-hui College of Chinese Medicine, Hefei 230038, China.
Zhen Ci Yan Jiu. 2008 Aug;33(4):240-4.
To explore the underlying mechanism of electroacupuncture (EA) in relieving morphine withdrawal syndrome in rats.
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.
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).
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.
探讨电针缓解大鼠吗啡戒断综合征的潜在机制。
将40只SD大鼠随机分为正常对照组、模型组1、模型组2和电针组。通过在后肢肌肉注射吗啡(第1天5mg/kg,每天递增直至第20天100mg/kg)建立吗啡戒断综合征模型。然后,模型组1的大鼠在第21天麻醉(10%水合氯醛)后处死,模型组2的大鼠在第27天处死。电针(2/100Hz,2 - 4mA)双侧“足三里”(ST36)30分钟,每天1次,共7天。(麻醉后)取出大鼠胸腺,切成切片(4μm),采用免疫组化方法染色以显示凋亡促进因子Bax、Fas、Fas配体(FasL)以及抗凋亡肽Bcl-2的表达。
与正常组相比,模型组1和模型组2的Bcl-2免疫反应(IR)阳性细胞数显著减少,而两个模型组的Bax、Fas和FasL IR阳性细胞数以及Bax/Bcl-2显著增加(P < 0.01)。与模型组2相比,模型组1的Bcl-2 IR阳性细胞数显著减少(P < 0.05),模型组1的Bax、Fas和FasL IR阳性细胞数以及Bax/Bcl-2显著更高(P < 0.01,P < 0.05)。电针后,与模型组2相比,电针组的Fas和FasL IR阳性细胞数以及Bax/Bcl-2显著减少(P < 0.01,P < 0.05),Bcl-2 IR阳性细胞数显著增加(P < 0.05);与模型组1相比,电针组的Bcl-2 IR阳性细胞数显著增加(P < 0.01),而Bax、Fas和FasL IR阳性细胞数以及Bax/Bcl-2明显减少(P < 0.01)。
电针“足三里”(ST36)可抑制吗啡诱导的Bcl-2下调以及Fas和FasL表达上调,这可能有助于其抵抗吗啡戒断大鼠胸腺细胞凋亡的作用。