Xu Ming-min, Zhang Dan-mei, Shi Rong-xing, Zhang Xu-hui, Wang Yu, Yu Miao, Guo Yu, Zhang Chun-tao, Zhao Bing-cong, Wu Ji-hong, Wu Ji-hong
Zhen Ci Yan Jiu. 2016 Apr;41(2):138-43.
To observe the effect of electroacupuncture (EA) on behavior changes and the adundance levels of transforming growth factor beta 3 (TGF-beta 3) and basic fibroblast growth factor (bFGF) proteins in the hippocampus of rats with chronic unpredictable mild stress (CUMS)-induced depression, so as to explore its mechanisms underlying improvement of depression.
Forty Sprague-Dawley rats were randomly divided into the following groups: control, model, EA, and medication (Fluoxetine), n = 10 in each group. The depression model was established by CUMS combined with solitary raising for 28 days. EA (2 Hz, 0.6 mA) was applied to "Baihui" (GV 20) and "Yintang" (GV 29) for 20 mm, once daily before CUMS every day. The rats of the medication group were given with Fluoxetine (10 mg/kg, 5 mL/kg) before CUMS every day. The behavioral changes (crossing and rearing locomotion) were detected by using open field tests. The expression levels of TGF-beta 3 and bFGF proteins of the bilateral hippocampus tissues were detected using biotin label-based antibody protein chips. Results Compared to the control group, the crossed grid-square numbers and rearing times were significantly decreased in the model group (P<0.01). Following EA and medication interventions, the CUMS induced decreases of the crossed grid-square number and rearing times were notably reversed in both EA and medication groups (P<0.01), suggesting an amelioration of depression after the intervention. The relative expression level of hippocampal TGF-beta 3 was down-regulated (fold change = 0.48, vs. the control group) and that of bFGF up-regulated (fold change= 1.36, vs the control group) in the model group. In both the EA and medication groups, the down-regulated TGF-beta 3 expression and the up-regulated bFGF protein expression were suppressed (TGF-beta 3: fold change = 1.61, 1.6 and bFGF: fold change = 0.61, 0.45, vs. the model group respectively).
EA can improve the depression-like state in depression rats which may be associated with its effect in up-regulating hippocampal TGF-beta 3 protein level and down-regulating bFGF protein expression via promoting neurogenesis.
观察电针（EA）对慢性不可预测性温和应激（CUMS）诱导的抑郁大鼠行为变化及海马组织中转化生长因子β3（TGF-β3）和碱性成纤维细胞生长因子（bFGF）蛋白表达水平的影响，以探讨其改善抑郁的作用机制。
将40只Sprague-Dawley大鼠随机分为对照组、模型组、电针组和药物组（氟西汀），每组10只。采用CUMS结合单笼饲养28天建立抑郁模型。电针组于每天进行CUMS前，取“百会”（GV 20）和“印堂”（GV 29）穴位，以2 Hz、0.6 mA强度电针刺激20分钟，每日1次。药物组于每天进行CUMS前给予氟西汀（10 mg/kg，5 mL/kg）灌胃。采用旷场试验检测大鼠行为变化（穿越格数和直立次数）。采用基于生物素标记的抗体蛋白芯片检测双侧海马组织中TGF-β3和bFGF蛋白的表达水平。结果与对照组相比，模型组大鼠穿越格数和直立次数显著减少（P<0.01）。电针和药物干预后，电针组和药物组大鼠CUMS诱导的穿越格数和直立次数减少均明显逆转（P<0.01），提示干预后抑郁状态得到改善。模型组海马TGF-β3相对表达水平下调（倍数变化=0.48，与对照组相比），bFGF相对表达水平上调（倍数变化=1.36，与对照组相比）。电针组和药物组中，下调的TGF-β3表达和上调的bFGF蛋白表达均受到抑制（TGF-β3：倍数变化分别为1.61、1.6，bFGF：倍数变化分别为0.61、0.45，与模型组相比）。
电针可改善抑郁大鼠的抑郁样状态，其机制可能与上调海马TGF-β3蛋白水平、下调bFGF蛋白表达、促进神经发生有关。
