自发性糖尿病大鼠的抑郁症行为与钙网织蛋白前体、原肌球蛋白1、细胞分裂素活化蛋白激酶1和活化分裂素蛋白激酶1表达的关联
|
摘要
目的探讨自发性糖尿病大鼠的抑郁症行为与钙网织蛋白前体、原肌球蛋白1、细胞分裂素活化蛋白激酶1和活化分裂素蛋白激酶1表达的关联。方法本研究以20只成年雄性健康大鼠(对照组)、40只自发性糖尿病大鼠为研究对象,采用随机数字法将40只自发性糖尿病大鼠分为糖尿病组与糖尿病抑郁组,糖尿病抑郁组受试大鼠构建抑郁模型。采用蔗糖水消耗试验、旷野试验测定3组受试大鼠抑郁行为,采用Western法测定3组受试大鼠海马组织中钙网织蛋白前体、原肌球蛋白1、细胞分裂素活化蛋白激酶1和活化分裂素蛋白激酶1表达水平。结果应激第15、22日,糖尿病抑郁组受试大鼠饮用蔗糖水量明显低于对照组及糖尿病组(P <0.05),对照组与糖尿病组差异无统计学意义(P> 0.05)。糖尿病抑郁组受试大鼠旷野试验水平得分、垂直得分均明显低于对照组及糖尿病组(P <0.05),对照组与糖尿病组差异无统计学意义(P> 0.05)。糖尿病抑郁组受试大鼠海马组织中钙网织蛋白前体、原肌球蛋白1、细胞分裂素活化蛋白激酶1、活化分裂素蛋白激酶1表达量明显低于对照组及糖尿病组(P <0.05),对照组与糖尿病组差异无统计学意义(P> 0.05)。结论自发性糖尿病大鼠的抑郁症行为与大鼠海马组织中钙网织蛋白前体、原肌球蛋白1、细胞分裂素活化蛋白激酶1、活化分裂素蛋白激酶1表达水平下降相关。
Objective To investigate the association between depression behavior and the expression of calreticulin precursor, tropomyosin I, milogen activated prolein kinase 1 and dual specificity mitogen-activated protein kinase 1 in spontaneous diabetes mellitus rats. Methods Twenty adult male healthy rats(control group) and 40 spontaneous diabetic rats were studied. Forty spontaneous diabetic rats were further divided into diabetes group and diabetic depression group, and the latter was to construct depression model. The depressive behavior of the 3 groups was measured by sucrose water consumption test and wilderness test. The expression level of calreticulin precursor, tropomyosin 1, milogen activated prolein kinase 1, and dual specificity mitogen-activated protein kinase 1 in the hippocampus of the 3 groups was measured by western blot. Results In the 15 th day and 22 nd days of stress,the amount of sucrose water drinking of the rats in diabetic depression group was significantly lower than that of the control group and the diabetes group(P < 0.05), and there was no significant difference between the control group and the diabetic group(P > 0.05). The score of field test and vertical score in the diabetic depression group were significantly lower than those of the control group and the diabetes group(P < 0.05), but there was no significant difference between the control group and the diabetic group(P > 0.05). The expression of calreticulin precursor,tropomyosin 1, milogen activated prolein kinase 1, and dual specificity mitogen-activated protein kinase 1 in the hippocampus of diabetic depression group was significantly lower than that in the control group and the diabetic group(P < 0.05), and there was no significant difference between the control group and the diabetic group(P > 0.05).Conclusions The depressive behavior of spontaneously diabetic rats is associated with the decrease of the expression level of calreticulin precursor, tropomyosin 1, milogen activated prolein kinase 1, and dual specificity mitogenactivated protein kinase 1 in the hippocampus of rats.
Objective To investigate the association between depression behavior and the expression of calreticulin precursor, tropomyosin I, milogen activated prolein kinase 1 and dual specificity mitogen-activated protein kinase 1 in spontaneous diabetes mellitus rats. Methods Twenty adult male healthy rats(control group) and 40 spontaneous diabetic rats were studied. Forty spontaneous diabetic rats were further divided into diabetes group and diabetic depression group, and the latter was to construct depression model. The depressive behavior of the 3 groups was measured by sucrose water consumption test and wilderness test. The expression level of calreticulin precursor, tropomyosin 1, milogen activated prolein kinase 1, and dual specificity mitogen-activated protein kinase 1 in the hippocampus of the 3 groups was measured by western blot. Results In the 15 th day and 22 nd days of stress,the amount of sucrose water drinking of the rats in diabetic depression group was significantly lower than that of the control group and the diabetes group(P < 0.05), and there was no significant difference between the control group and the diabetic group(P > 0.05). The score of field test and vertical score in the diabetic depression group were significantly lower than those of the control group and the diabetes group(P < 0.05), but there was no significant difference between the control group and the diabetic group(P > 0.05). The expression of calreticulin precursor,tropomyosin 1, milogen activated prolein kinase 1, and dual specificity mitogen-activated protein kinase 1 in the hippocampus of diabetic depression group was significantly lower than that in the control group and the diabetic group(P < 0.05), and there was no significant difference between the control group and the diabetic group(P > 0.05).Conclusions The depressive behavior of spontaneously diabetic rats is associated with the decrease of the expression level of calreticulin precursor, tropomyosin 1, milogen activated prolein kinase 1, and dual specificity mitogenactivated protein kinase 1 in the hippocampus of rats.
引文
[1]田朝阳,图娅,姜会梨,等.电针对慢性应激抑郁模型大鼠海马及血清caspase-12表达的影响[J].北京中医药大学学报,2018,41(2):154-159.
[2]WANG Y,CHANG T,CHEN Y C,et al.Quetiapine add-on therapy improves the depressive behaviors and hippocampal neurogenesis in fluoxetine treatment resistant depressive rats[J].Behav Brain Res,2013,253:206-211.
[3]吴永胜,万平新,万顺梅,等.舒肝解郁胶囊治疗进展期胃癌并发抑郁症的临床研究[J].现代消化及介入诊疗,2014,19(3):150-152.
[4]孙宏伟,李承德,毛淑梅,等.支气管哮喘伴发抑郁大鼠模型的建立[J].中国实验动物学报,2010,18(2):156-160.
[5]饶冬萍,陈建华,温全球,等.5-羟色胺1A受体C(-1019)G基因多态性与老年抑郁症和伴有抑郁症状的阿尔茨海默病的关联研究[J].实用医学杂志,2014,30(5):758-760.
[6]TANG M M,LIN W J,PAN Y Q,et al.Hippocampal neurogenesis dysfunction linked to depressive-like behaviors in a neuroinflammation induced model of depression[J].Physiol Behav,2016,161:166-173.
[7]HU P,WANG Y,LIU J,et al.Chronic retinoic acid treatment suppresses adult hippocampal neurogenesis,in close correlation with depressive-like behavior[J].Hippocampus,2016,26(7):911-923.
[8]GAGAT M,GRZANKA D,IZDEBSKA M,et al.Effect of L-homocysteine on endothelial cell-cell junctions following F-actin stabilization through tropomyosin-1 overexpression[J].Int JMol Med,2013,32(1):115-129.
[9]李臻琰.脑红蛋白及热休克蛋白60在脑挫裂伤病理过程中的作用研究[D].中南大学,2012.
[10]张贵锋,吴晓玲,曾统军,等.通元针法联合隔药盐灸神阙对产后抑郁大鼠行为和下丘脑-垂体-肾上腺轴的影响[J].实用医学杂志,2018,34(8):1262-1266.
[11]汤光花,陈永新,张瑞岭.舒肝颗粒对抑郁大鼠海马神经元凋亡、脑组织caspase-3蛋白及外周血中细胞因子水平的影响[J].中国老年学杂志,2018,38(1):52-54.
[12]YAMAUCHI N,HARADA T,TANIGUCHI F,et al.肿瘤坏死因子-α通过核因子-κB和细胞分裂素活化蛋白激酶途径诱导异位子宫内膜基质细胞释放白细胞介素-6[J].世界核心医学期刊文摘(妇产科学分册),2005(3):25.
[13]XU H J,JIANG W D,FENG L,et al.Dietary vitamin C deficiency depressed the gill physical barriers and immune barriers referring to Nrf2,apoptosis,MLCK,NF-κB and TOR signaling in grass carp(Ctenopharyngodon idella)under infection of Flavobacterium columnare[J].Fish Shellfish Immunol,2016,58:177-192.
[14]LI L,FENG L,JIANG W D,et al.Dietary pantothenic acid depressed the gill immune and physical barrier function via NF-κB,TOR,Nrf2,p38MAPK and MLCK signaling pathways in grass carp(Ctenopharyngodon idella)[J].Fish Shellfish Immunol,2015,47(1):500-510.
[15]李明娜,张炜明,曹海龙,等.原肌球蛋白1在非小细胞肺癌中的表达及意义[J].江苏医药,2010,36(18):2133-2136,2108.
[16]LAJUD N,GONZALEZ-ZAPIEN R,ROQUE A,et al.Prolactin administration during early postnatal life decreases hippocampal and olfactory bulb neurogenesis and results in depressive-like behavior in adulthood[J].Horm Behav,2013,64(5):781-789.
[17]罗乐.针刺调节抑郁大鼠海马AMPA受体及突触相关蛋白表达的研究[D].广州中医药大学,2017.
[18]KREISEL T,FRANK M G,LICHT T,et al.Dynamic microglial alterations underlie stress-induced depressive-like behavior and suppressed neurogenesis[J].Mol Psychiatry,2014,19(6):699-709.
[2]WANG Y,CHANG T,CHEN Y C,et al.Quetiapine add-on therapy improves the depressive behaviors and hippocampal neurogenesis in fluoxetine treatment resistant depressive rats[J].Behav Brain Res,2013,253:206-211.
[3]吴永胜,万平新,万顺梅,等.舒肝解郁胶囊治疗进展期胃癌并发抑郁症的临床研究[J].现代消化及介入诊疗,2014,19(3):150-152.
[4]孙宏伟,李承德,毛淑梅,等.支气管哮喘伴发抑郁大鼠模型的建立[J].中国实验动物学报,2010,18(2):156-160.
[5]饶冬萍,陈建华,温全球,等.5-羟色胺1A受体C(-1019)G基因多态性与老年抑郁症和伴有抑郁症状的阿尔茨海默病的关联研究[J].实用医学杂志,2014,30(5):758-760.
[6]TANG M M,LIN W J,PAN Y Q,et al.Hippocampal neurogenesis dysfunction linked to depressive-like behaviors in a neuroinflammation induced model of depression[J].Physiol Behav,2016,161:166-173.
[7]HU P,WANG Y,LIU J,et al.Chronic retinoic acid treatment suppresses adult hippocampal neurogenesis,in close correlation with depressive-like behavior[J].Hippocampus,2016,26(7):911-923.
[8]GAGAT M,GRZANKA D,IZDEBSKA M,et al.Effect of L-homocysteine on endothelial cell-cell junctions following F-actin stabilization through tropomyosin-1 overexpression[J].Int JMol Med,2013,32(1):115-129.
[9]李臻琰.脑红蛋白及热休克蛋白60在脑挫裂伤病理过程中的作用研究[D].中南大学,2012.
[10]张贵锋,吴晓玲,曾统军,等.通元针法联合隔药盐灸神阙对产后抑郁大鼠行为和下丘脑-垂体-肾上腺轴的影响[J].实用医学杂志,2018,34(8):1262-1266.
[11]汤光花,陈永新,张瑞岭.舒肝颗粒对抑郁大鼠海马神经元凋亡、脑组织caspase-3蛋白及外周血中细胞因子水平的影响[J].中国老年学杂志,2018,38(1):52-54.
[12]YAMAUCHI N,HARADA T,TANIGUCHI F,et al.肿瘤坏死因子-α通过核因子-κB和细胞分裂素活化蛋白激酶途径诱导异位子宫内膜基质细胞释放白细胞介素-6[J].世界核心医学期刊文摘(妇产科学分册),2005(3):25.
[13]XU H J,JIANG W D,FENG L,et al.Dietary vitamin C deficiency depressed the gill physical barriers and immune barriers referring to Nrf2,apoptosis,MLCK,NF-κB and TOR signaling in grass carp(Ctenopharyngodon idella)under infection of Flavobacterium columnare[J].Fish Shellfish Immunol,2016,58:177-192.
[14]LI L,FENG L,JIANG W D,et al.Dietary pantothenic acid depressed the gill immune and physical barrier function via NF-κB,TOR,Nrf2,p38MAPK and MLCK signaling pathways in grass carp(Ctenopharyngodon idella)[J].Fish Shellfish Immunol,2015,47(1):500-510.
[15]李明娜,张炜明,曹海龙,等.原肌球蛋白1在非小细胞肺癌中的表达及意义[J].江苏医药,2010,36(18):2133-2136,2108.
[16]LAJUD N,GONZALEZ-ZAPIEN R,ROQUE A,et al.Prolactin administration during early postnatal life decreases hippocampal and olfactory bulb neurogenesis and results in depressive-like behavior in adulthood[J].Horm Behav,2013,64(5):781-789.
[17]罗乐.针刺调节抑郁大鼠海马AMPA受体及突触相关蛋白表达的研究[D].广州中医药大学,2017.
[18]KREISEL T,FRANK M G,LICHT T,et al.Dynamic microglial alterations underlie stress-induced depressive-like behavior and suppressed neurogenesis[J].Mol Psychiatry,2014,19(6):699-709.