交泰丸对慢性温和不可预知性应激抑郁模型大鼠炎性细胞因子的影响
|
摘要
目的探讨交泰丸对慢性温和不可预知性应激(CUMS)抑郁模型大鼠致炎、抗炎细胞因子的影响。方法大鼠采用CUMS方法制备抑郁模型,比较体质量变化,进行糖水消耗实验和开场实验;并采用酶联免疫吸附测定法(ELISA)测定大鼠血清及海马组织中炎性细胞因子白细胞介素(IL)-1β、IL-6、肿瘤坏死因子(TNF)-α、IL-4、IL-10的水平,尼氏染色法观察大鼠海马神经元形态。结果与对照组比较,模型组大鼠糖水消耗量、穿越横格数和直立次数均明显减少;血清及海马内IL-1β、IL-6、TNF-α、IL-4明显升高,IL-10明显降低;海马神经元分层不清,排列紊乱,尼氏体浅染或消失。与模型组比较,交泰丸给药组大鼠糖水消耗量、穿越横格数和直立次数均明显增加;血清及海马内IL-1β、IL-6、TNF-α明显降低,IL-4、IL-10明显升高;海马神经元分层较明显,尼氏体浅染。结论交泰丸可明显改善大鼠抑郁样行为及海马神经元损伤,其机制可能与下调血清及海马致炎细胞因子IL-1β、IL-6、TNF-α和上调抗炎细胞因子IL-4、IL-10表达有关。
Objective To study the mechanism of Jiaotai Pill on inflammation and anti-inflammatory cytokines in mice with chronic unpredictable mild stress(CUMS) depression. Methods Mice were treated with CUMS depression model, then the weight comparison, sugar test, opening experiment was conducted; The levels of IL-1β, IL-6 and TNF-α, IL-4, and IL-10 in the serum and hippocampus of rats were measured by enzyme-linked immunosorbent assay(ELISA), and rat hippocampal neuron morphology was observed by Nissl's staining. Results Compared with the blank group, the consumption of sugar, the number of crosses and the number of vertical bars in the model group were significantly decreased; The levels of IL-1β, IL-6, TNF-α, and IL-4 in serum and hippocampus were significantly higher than those in the blank group, and IL-10 significantly reduced; Hippocampal neurons stratified unclear, arranged disorder, Nissie shallow staining or disappear. Compared with the model group, the consumption of sugar, the number of crosses and the number of vertical bars in Jiaotai Pill administration group were significantly increased; The levels of IL-1β, IL-6, and TNF-α in serum and hippocampus were significantly decreased, and the levels of IL-4 and IL-10 was significantly increased; Hippocampal neuronal stratification was more obvious, Nissl shallow staining. Conclusion Jiaotai Pill can significantly improve the behavior of rat depression and hippocampal neuronal injury whose mechanism may be related to down-regulation of serum and hippocampus proinflammatory cytokines IL-1β, IL-6, TNF-α, up-regulation of anti-inflammatory cytokines IL-4 and IL-10.
Objective To study the mechanism of Jiaotai Pill on inflammation and anti-inflammatory cytokines in mice with chronic unpredictable mild stress(CUMS) depression. Methods Mice were treated with CUMS depression model, then the weight comparison, sugar test, opening experiment was conducted; The levels of IL-1β, IL-6 and TNF-α, IL-4, and IL-10 in the serum and hippocampus of rats were measured by enzyme-linked immunosorbent assay(ELISA), and rat hippocampal neuron morphology was observed by Nissl's staining. Results Compared with the blank group, the consumption of sugar, the number of crosses and the number of vertical bars in the model group were significantly decreased; The levels of IL-1β, IL-6, TNF-α, and IL-4 in serum and hippocampus were significantly higher than those in the blank group, and IL-10 significantly reduced; Hippocampal neurons stratified unclear, arranged disorder, Nissie shallow staining or disappear. Compared with the model group, the consumption of sugar, the number of crosses and the number of vertical bars in Jiaotai Pill administration group were significantly increased; The levels of IL-1β, IL-6, and TNF-α in serum and hippocampus were significantly decreased, and the levels of IL-4 and IL-10 was significantly increased; Hippocampal neuronal stratification was more obvious, Nissl shallow staining. Conclusion Jiaotai Pill can significantly improve the behavior of rat depression and hippocampal neuronal injury whose mechanism may be related to down-regulation of serum and hippocampus proinflammatory cytokines IL-1β, IL-6, TNF-α, up-regulation of anti-inflammatory cytokines IL-4 and IL-10.
引文
[1]刘佳莉,苑玉和,陈乃宏,等.抑郁症的治疗研究进展[J].中国药理学通报,2011,27(9):1193-1196.
[2]Belmaker R H,Agam G.Major depression discover[J].NEngl J Med,2008,358(1):55-68.
[3]熊志明.配伍肉桂醛对盐酸小檗碱在快速动眼睡眠剥夺大鼠血液与脑组织分布的影响[D].广州:广州中医药大学,2015.
[4]王秋,方志军.不同比例交泰丸镇静催眠作用的药效学研究[J].中医临床研究,2011,3(11):16-17.
[5]张月月,王君明,崔瑛,等.中药生物碱类成分抗焦虑或抑郁活性及黄连生物碱药理作用研究进展[J].中华中医药杂志,2015,30(4):1184-1187.
[6]吴存恩,王瑞平,滕钰浩.肉桂活性成分及抗肿瘤作用研究进展[J].时珍国医国药,2015,26(8):1985-1987.
[7]于春泉,王怡,高杉,等.交泰丸不同配比抗抑郁作用的实验研究[J].中国实验方剂学杂志,2012,18(6):225-228.
[8]于泽胜,潘晔,宋彦奇,等.交泰丸对利血平诱导小鼠抑郁模型的影响[J].天津中医药,2016,33(12):740-744.
[9]杨帅,潘晔,宋彦奇,等.交泰丸对抑郁大鼠行为学及脑内单胺类神经递质的影响[J].中草药,2016,47(23):4218-4223.
[10]Maes M.Evidence for an immune response in major depression:A review and hypothesis[J].Prog Neuropsychopharmacol Biol Psychiatry,1995,19(1):11-38.
[11]Lichtblau N,Schmidt F M,Schumann R,et al.Cytokines as biomarkers in depressive disorder:current standing and prospects[J].Int Rev Psychiat,2013,25(5):592-603.
[12]Patel A.Review:the role of inflammation in depression[J].Psychiatria Danubina,2013,25(2):216-223.
[13]王东林,林文娟.细胞因子与抑郁症发病机制研究进展[J].中国神经精神疾病杂志,2007,33(9):572-574.
[14]You Z L,Luo C M,Zhang W Z,et al.Pro-and antiinflammatory cytokines expression in rat’s brain and spleen exposed to chronic mild stress:Involvement in depression[J].Behav Brain Res,2011,225(1):135-141.
[15]徐说,林文娟.抗炎性细胞因子与抑郁症[J].生物化学与生物物理进展,2014,41(11):1099-1108.
[16]Henry C J,Yan H,Wynne A,et al.Minocycline attenuates lipopolysaccharide(LPS)-induced neuroinflammation,sickness behavior,and anhedonia[J].J Neuroinflam,2008,5(1):15.
[17]邓朔,张鸿燕.抑郁症发病机制的神经免疫相关靶点研究现状[J].中国临床药理学杂志,2017,33(3):280-283.
[18]张敏,于春泉.交泰丸抗抑郁作用的研究进展[J].天津中医药,2012,29(1):101-104.
[2]Belmaker R H,Agam G.Major depression discover[J].NEngl J Med,2008,358(1):55-68.
[3]熊志明.配伍肉桂醛对盐酸小檗碱在快速动眼睡眠剥夺大鼠血液与脑组织分布的影响[D].广州:广州中医药大学,2015.
[4]王秋,方志军.不同比例交泰丸镇静催眠作用的药效学研究[J].中医临床研究,2011,3(11):16-17.
[5]张月月,王君明,崔瑛,等.中药生物碱类成分抗焦虑或抑郁活性及黄连生物碱药理作用研究进展[J].中华中医药杂志,2015,30(4):1184-1187.
[6]吴存恩,王瑞平,滕钰浩.肉桂活性成分及抗肿瘤作用研究进展[J].时珍国医国药,2015,26(8):1985-1987.
[7]于春泉,王怡,高杉,等.交泰丸不同配比抗抑郁作用的实验研究[J].中国实验方剂学杂志,2012,18(6):225-228.
[8]于泽胜,潘晔,宋彦奇,等.交泰丸对利血平诱导小鼠抑郁模型的影响[J].天津中医药,2016,33(12):740-744.
[9]杨帅,潘晔,宋彦奇,等.交泰丸对抑郁大鼠行为学及脑内单胺类神经递质的影响[J].中草药,2016,47(23):4218-4223.
[10]Maes M.Evidence for an immune response in major depression:A review and hypothesis[J].Prog Neuropsychopharmacol Biol Psychiatry,1995,19(1):11-38.
[11]Lichtblau N,Schmidt F M,Schumann R,et al.Cytokines as biomarkers in depressive disorder:current standing and prospects[J].Int Rev Psychiat,2013,25(5):592-603.
[12]Patel A.Review:the role of inflammation in depression[J].Psychiatria Danubina,2013,25(2):216-223.
[13]王东林,林文娟.细胞因子与抑郁症发病机制研究进展[J].中国神经精神疾病杂志,2007,33(9):572-574.
[14]You Z L,Luo C M,Zhang W Z,et al.Pro-and antiinflammatory cytokines expression in rat’s brain and spleen exposed to chronic mild stress:Involvement in depression[J].Behav Brain Res,2011,225(1):135-141.
[15]徐说,林文娟.抗炎性细胞因子与抑郁症[J].生物化学与生物物理进展,2014,41(11):1099-1108.
[16]Henry C J,Yan H,Wynne A,et al.Minocycline attenuates lipopolysaccharide(LPS)-induced neuroinflammation,sickness behavior,and anhedonia[J].J Neuroinflam,2008,5(1):15.
[17]邓朔,张鸿燕.抑郁症发病机制的神经免疫相关靶点研究现状[J].中国临床药理学杂志,2017,33(3):280-283.
[18]张敏,于春泉.交泰丸抗抑郁作用的研究进展[J].天津中医药,2012,29(1):101-104.