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[电针对慢性应激抑郁大鼠海马细胞凋亡及JNK信号通路的影响]

[Effect of electroacupuncture on hippocampal apoptosis and JNK signal pathway in chronic stress depression rats].

作者信息

Dai Wei, Li Wei-Dong, Lu Jun

机构信息

College of Acu-moxibustion and Massage, Beijing University of Chinese Medicine, Beijing 100029, China.

出版信息

Zhen Ci Yan Jiu. 2010 Oct;35(5):330-4.

Abstract

OBJECTIVE

To observe the effect of electroacupuncture (EA) on hippocampal apoptosis and c-Jun N-terminal kinase (JNK) signal pathway in chronic stress depression rats so as to study its mechanism underlying acupuncture-induced improvement of depression.

METHODS

Sixty-five SD rats were randomly divided into control, control + EA, model, EA and Prozac groups, with 13 rats in each. Open-field test was used to detect the rats' behavior changes. The apoptotic rate of the hippocampal cells was detected by Annexin V fluorescein isothiocyanate (FITC)/ Propidium iodide (PI) (Annexin V-FITC/PI) double-staining, and the expression of hippocampal JNK protein detected by Western blot.

RESULTS

After repeated stress stimulation (21 days), the crossing numbers (1.8 +/- 0.2) and rearing times (0.5 +/- 0.01) in the model group were apparently lower than those (48.1 +/- 18.3, 14.2 +/- 2.4) in the control group and those (47.2 +/- 15.8, 13.5 +/- 2.6) in the control + EA group (P < 0.05). Compared with the model group, the crossing numbers and rearing times (40.2 +/- 10.1, 10.3 +/- 2.2) during 3 min in the EA group and those (39.8 +/- 12.4, 10.6 +/- 3.2) in the Prozac group were increased considerably (P < 0.05). The hippocampal apoptotic rate was significantly higher in the model group (67 +/- 10) than in the control (53 +/- 13) and control + EA groups (52 +/- 10, P < 0.05). In comparison with the model group, the apoptotic rate (29 +/- 9) of the EA group and that (51 +/- 13) of the Prozac group were significantly lower (P < 0.05). Compared with the control group, the phosphorylated JNK (p-JNK) level was considerably higher in the model group (P < 0.05); while compared with the model group, the p-JNK level was significantly lower in the EA and Pozac groups (P < 0.05). No apparent differences were found between the EA and and Prozac groups in the aforementioned indexes (P > 0.05).

CONCLUSION

EA can reduce hippocampal apoptotic rate and down-regulate hippocampal p-JNK level in depression rats, which is responsible for its effect in improving depression-induced decreased movement.

摘要

目的

观察电针(EA)对慢性应激抑郁大鼠海马细胞凋亡及c-Jun氨基末端激酶(JNK)信号通路的影响,以探讨针刺改善抑郁的作用机制。

方法

将65只SD大鼠随机分为对照组、对照+EA组、模型组、EA组和氟西汀组,每组13只。采用旷场试验检测大鼠行为变化。采用膜联蛋白V异硫氰酸荧光素(FITC)/碘化丙啶(PI)(Annexin V-FITC/PI)双染法检测海马细胞凋亡率,采用蛋白质免疫印迹法检测海马JNK蛋白表达。

结果

重复应激刺激(21天)后,模型组的穿越次数(1.8±0.2)和直立次数(0.5±0.01)明显低于对照组(48.1±18.3,14.2±2.4)和对照+EA组(47.2±15.8,13.5±2.6)(P<0.05)。与模型组相比,EA组3分钟内的穿越次数和直立次数(40.2±10.1,10.3±2.2)以及氟西汀组(39.8±12.4,10.6±3.2)显著增加(P<0.05)。模型组海马凋亡率(67±10)显著高于对照组(53±13)和对照+EA组(52±10,P<0.05)。与模型组相比,EA组凋亡率(29±9)和氟西汀组(51±13)显著降低(P<0.05)。与对照组相比,模型组磷酸化JNK(p-JNK)水平显著升高(P<0.05);与模型组相比,EA组和氟西汀组p-JNK水平显著降低(P<0.05)。EA组与氟西汀组上述指标比较差异无统计学意义(P>0.05)。

结论

电针可降低抑郁大鼠海马凋亡率,下调海马p-JNK水平,这可能是其改善抑郁所致运动减少的作用机制。

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