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Expression and interaction of TNF-α and VEGF in chronic stress-induced depressive rats

机译：TNF-α和VEGF在慢性应激性抑郁大鼠中的表达及相互作用

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The incidence of depression increases annually but the pathogenesis is not yet fully understood. The aim of the present study was to explore the expression and interaction of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in chronic stress-induced depressive rats. A total of 20 adult healthy Sprague Dawley rats (180–220 g) were randomly divided into the control and experimental depression groups. The depression model was established with a chronic stress method, and the success of model construction was assessed through weigh measurements and the sugar consumption and open-field tests. The expression of TNF-α and VEGF was detected using the reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blotting and immunohistochemistry. Compared with the control group, the weight of the rats in the experimental group was found to be reduced (P<0.05). The open-field test showed significant differences in the horizontal and vertical motion of the rats between the two groups, and the rats in the experimental group exhibited a significantly reduced ability to adapt to a new environment (P<0.05). Furthermore, the sensitivity of the rats in the experimental group to reward stimulation was decreased. The relative mRNA expression levels of TNF-α and VEGF in the hippocampus of the experimental group were lower than those in the control group, and western blot analysis revealed that the protein expression of VEGF and TNF-α was reduced in the experimental group. Neurons of the experimental group exhibited reduced immunohistochemical staining compared with neurons from the normal hippocampus in the control group. In conclusion, the present study investigated the association between the occurrence of depression and TNF-α and VEGF at the mRNA and protein levels using RT-qPCR, western blotting, immunohistochemistry and animal behavior experiments. The results provide a fundamental basis for follow-up clinical research.
机译：抑郁症的发病率逐年增加，但发病机理尚未完全明了。本研究的目的是探讨肿瘤坏死因子-α（TNF-α）和血管内皮生长因子（VEGF）在慢性应激诱导的抑郁大鼠中的表达和相互作用。总共20只成年健康Sprague Dawley大鼠（180-220 g）随机分为对照组和实验抑郁组。通过慢性压力法建立了抑郁症模型，并通过称重测量，糖消耗和露天试验评估了模型构建的成功性。逆转录定量聚合酶链反应（RT-qPCR），蛋白质印迹和免疫组化检测TNF-α和VEGF的表达。与对照组相比，实验组大鼠体重减轻（P <0.05）。野外试验显示两组大鼠水平和垂直运动之间存在显着差异，实验组大鼠适应新环境的能力显着降低（P <0.05）。此外，实验组中的大鼠对奖励刺激的敏感性降低。实验组海马中TNF-α和VEGF的相对mRNA表达水平低于对照组，Western blot分析显示实验组海马中TNF和α-VEGF的蛋白表达降低。与对照组正常海马神经元相比，实验组神经元免疫组化染色减少。总之，本研究使用RT-qPCR，western印迹，免疫组织化学和动物行为实验研究了抑郁症的发生与mRNA和蛋白质水平上TNF-α和VEGF之间的关系。研究结果为后续临床研究提供了基础。

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