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生品与麸炒苍术对脾虚证大鼠结肠及胰腺磷酸化钙调素依赖蛋白激酶Ⅱ的影响

The Effects of Raw and Bran-fried Rhizoma Atractylodes on Calmodulin-related Signaling Pathway of Colon and Pancreas in Rats with Spleen Deficiency Syndrome
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摘要 目的通过比较苍术麸炒前后影响脾虚证大鼠结肠及胰腺磷酸化钙调素依赖蛋白激酶Ⅱ(p-CaMKⅡ)信号通路相关蛋白表达的差异,探讨苍术麸炒后健脾作用的机制。方法雄性SD大鼠70只随机分为正常组、脾虚证模型组(以下简称模型组)、生苍术(高、低)剂量组、麸炒苍术(高、低)剂量组、复方谷氨酰胺组,复制脾虚模型后相应剂量药物灌胃治疗。治疗期满后观察各组大鼠结肠及胰腺组织病理学改变,并检测结肠、胰腺组织细胞中Ca^(2+)表达水平与结肠、胰腺组织中p-CaMKⅡ蛋白和基因表达。结果造模结束时,光镜观察,正常组大鼠结肠及胰腺形态组织学无明显异常,模型大鼠结肠黏膜上皮变性、坏死,肠绒毛上皮脱落,固有膜结构被破坏,胰腺组织胰岛数明显减少,细胞分布不均,岛内细胞大量呈空泡状;与正常组比较,模型组结肠组织细胞Ca^(2+)荧光值升高,胰腺组织细胞Ca^(2+)荧光值降低,结肠组织p-CaMKⅡ蛋白和基因表达水平升高,胰腺组织p-CaMKⅡ蛋白和基因表达水平降低(P<0.01);与模型组比较,各治疗组结肠及胰腺组织结构有不同程度修复,结肠组织细胞Ca^(2+)表达的荧光强度不同程度降低,胰腺组织细胞Ca^(2+)荧光值不同程度升高;结肠p-CaMKⅡ蛋白和基因表达降低,胰腺组织p-CaMKⅡ蛋白和基因表达水平升高(P<0.01);与生苍术(高、低)剂量组比较,麸炒苍术(高、低)剂量组上述指标改善更为明显(P<0.05或P<0.01)。结论苍术麸炒后可通过Ca^(2+)/p-CaMKⅡ信号途径更好调节和改善脾虚大鼠结肠、胰腺结构及功能并改善脾虚证候。 Objective By comparing the effects of raw and atractylosis fried with bran on p-CaMKⅡsignaling pathway related proteins in colon and pancreas tissue of rats with spleen deficiency syndrome,explore the mechanism of atractylosisFried with bran to improve gastrointestinal function.Methods 70 male SD rats were randomly divided into the normal group,spleen deficiency model group(hereinafter referred to as the model group),rhizoma atractylodis,high and low dose group,rhizoma atractylodis Fried with bran high and low dose group,compound glutamine group.The spleen-deficiency model was reproduced.After the modeling,each treatment group was given the corresponding dose of drugs by gavage.After the treatment,the histopathological changes of small intestine and pancreas were observed.the expression of Ca^(2+)in colon and pancreatic tissues,and the expression of p-CAMKⅡprotein and gene in colon and pancreatic tissues were detected.Results At the end of the building model,light microscopy observation,the morphology and histology of colon and pancreas in the normal group were normal;The intestinal mucosa epithelial degeneration,necrosis,intestinal villus epithelial shedding,intrinsic membrane structure of the model rat small was damaged,the pancreas islet number decreased significantly,cell distribution,a lot of island cell show vacuolated.Compared with the normal group,the expression of p-CaMKⅡprotein and gene were increased in the model group,while the fluorescence of ca^(2+)was increased in the colon and decreased in the pancreas,and the expression level of p-CaMKⅡprotein and gene in pancreatic tissue was decreased(P<0.01),and compared with the model group,the structure of colon and pancreas in each treatment group was repaired to different extent,the fluorescence intensity of ca^(2+)in colon tissue cells decreased,while that of pancreatic tissue cells increased,and the expression of p-CaMKⅡprotein and gene in colon decreased,the expression level of p-CaMKⅡprotein and gene in pancreatic tissue increased(P<0.01);C
作者 谢慧臣 罗丽华 吴广阳 XIE Huichen;LUO Lihua;WU Guangyang(Hubei University for Nationalities,Enshi 445000,China;Enshi Autonomous States Central Medicine Hospital,Enshi 445000,China)
出处 《湖北民族大学学报(医学版)》 2023年第3期25-29,共5页 Journal of Hubei Minzu University(Medical Edition)
基金 湖北省自然科学基金(2019CFB781)。
关键词 麸炒 苍术 脾虚 钙调蛋白/钙调素依赖蛋白激酶Ⅱ 磷酸化 bran-Fried Rhizoma Atractylodis Spleen Deficient Calmodulin/Calmodulin-Dependent Protein KinaseⅡ Phosphorylation
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