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尹丽红,焦琳,陈裕,陈嘉欣,杜斯琪,王翰林,赵舜滢,殷春霞,曹丽芬,余万霖,谢长才.多囊卵巢综合征大鼠子宫内膜中 PI3K/ AKT 通路 相关蛋白表达异常与胰岛素抵抗的关系[J].中国实验动物学报,2022,30(6):777~783.
多囊卵巢综合征大鼠子宫内膜中 PI3K/ AKT 通路 相关蛋白表达异常与胰岛素抵抗的关系
Relationship between abnormal expression of PI3K / AKT pathway-related protein and insulin resistance of rats of polycystic ovary syndrome with endometrial insulin resistance
投稿时间:2022-04-19  
DOI:10. 3969 / j.issn.1005-4847. 2022. 06. 006
中文关键词:  多囊卵巢综合征  胰岛素抵抗  脱氢表雄酮  高脂饮食  大鼠模型  子宫内膜
英文关键词:polycystic ovary syndrome  insulin resistance  dehydroepiandrosterone  high-fat diet  rat model  endometrial
基金项目:
作者单位
尹丽红 广州中医药大学第二临床医学院,广州 510006 
焦琳 广东省中医院,广州 510120 
陈裕 广东省中医院,广州 510120 
陈嘉欣 广州医科大学附属中医医院,广州 510130 
杜斯琪 广东省中医院,广州 510120 
王翰林 广东省中医院,广州 510120 
赵舜滢 广州中医药大学第二临床医学院,广州 510006 
殷春霞 广东省中医院,广州 510120 
曹丽芬 广东省中医院,广州 510120 
余万霖 广东省中医院,广州 510120 
谢长才 广东省中医院,广州 510120 
Author NameAffiliation
YIN Lihong the Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou 510006, China 
JIAO Lin Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120 
CHEN Yu Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120 
CHEN Jiaxin the Affiliated Traditional Chinese Medicine Hospital of Guangzhou Medical University, Guangzhou 510130 
DU Siqi Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120 
WANG Hanlin Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120 
ZHAO Shunying the Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou 510006, China 
YIN Chunxia Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120 
CAO Lifen Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120 
YU Wanlin Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120 
XIE Changcai Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120 
摘要点击次数: 120
全文下载次数: 26
中文摘要:
       目的 通过脱氢表雄酮(DHEA)联合高脂饮食(HFDs)构建多囊卵巢综合征(PCOS)子宫内膜局部胰岛素抵抗(IR)的大鼠模型,通过检测子宫内膜中胰岛素相关蛋白及 PI3K/ AKT 通路相关蛋白的表达水平,观察子宫内膜是否存在胰岛素抵抗并探究其可能机制。 方法 选取 32 只 21 日龄 SD 雌性大鼠,随机分为模型组( n= 24)与对照组(n= 8)。 模型组每天于颈背部皮下注射 DHEA 6 mg / 100 g 并以高脂饲料喂养,对照组于颈背部皮下 注射同等体积的注射用玉米油并以正常饲料喂养,实验周期 30 d。 根据阴道涂片及卵巢组织染色结果筛选出 PCOS 大鼠,通过检测空腹血糖(FBG)、血清胰岛素水平(FINS)、胰岛素抵抗指数(HOMA-IR)筛选出 PCOS 伴 IR 的大鼠(PCOS-IR 组),再通过检测其与对照组子宫内膜中 IR 相关蛋白( IRS1、GLUT-4)及 PI3K/ AKT 通路相关蛋白 (PI3K、PI3K p110α、p-AKT、AKT)的表达差异,探究其可能机制。 结果 对照组大鼠涂片示规律动情、卵巢组织结构正常,而模型组大鼠动情周期紊乱、卵巢符合多囊卵巢表现,且模型组大鼠与对照组比较,其 FBG(P> 0. 05)、 FINS(P> 0. 05)及 HOMA-IR 指数(P< 0. 01)均升高,其中从模型组筛选出 PCOS 大鼠 11 只,PCOS-IR 大鼠 8 只, 其中 6 只子宫内膜组织 IRS1、GLUT-4 表达水平显著降低(P< 0. 01),提示子宫内膜组织存在 IR。 此外,与对照组 相比,PCOS-IR 组子宫内膜组织中的 PI3K 表达水平上升(P< 0. 05),PI3K p110α(P< 0. 01)、p-AKT(P< 0. 01)及 AKT 表达水平(P> 0. 05)降低,提示子宫内膜中 PI3K/ AKT 通路相关蛋白表达下调。 结论 PCOS 伴 IR 大鼠其表 现特征性的多囊卵巢组织、糖代谢异常,其子宫内膜可能存在胰岛素抵抗,且可能与 PI3K/ AKT 通路相关蛋白表达异常有关。
英文摘要:
       Objective To establish a rat model of polycystic ovary syndrome (PCOS) with endometrial insulin resistance(IR) by combining dehydroepiandrosterone ( DHEA) with a high fat diet ( HFDs). And by detecting the expression levels of insulin resistance related proteins and PI3K/ AKT pathway-related proteins in the endometrium, we can observe whether there is insulin resistance in the endometrium and explore its possible mechanism. Methods Thirty-two 21-day-old SD female rats were randomly divided into a Model group (Model group, n= 24) and Control group (Control group, n= 8). The Model group was subcutaneously injected with 6 mg / 100 (g·d) DHEA on the back of the neck and fed the high fat diet. The Control group was subcutaneously injected with the same volume of corn oil for injection on the back of the neck and fed a normal diet. The experimental period was 30 days. In accordance with the result of vaginal smear and ovarian tissue staining, PCOS rats were screened. And PCOS with IR rats ( PCOS-IR) were screened by detecting fasting blood glucose (FBG), serum insulin level (FINS), and insulin resistance index (HOMA-IR). Then by detecting the differences in the expression of IR-related proteins (IRS1, GLUT-4) and PI3K/ AKT pathway-related proteins (PI3K, PI3K p110α, p-AKT, AKT) in the endometrium between the two groups to explore the possible mechanism. Results Smears from rats in the Control group showed regular estrus and a normal ovarian tissue structure, whereas those of rats in the Model group had disordered estrous cycles and the ovaries had polycystic ovary manifestations. Compared with the Control group, FBG (P> 0. 05), FINS (P> 0. 05), and HOMA-IR (P< 0. 01) of rats in the Model group were all increased, among which 11 PCOS rats and eight PCOS with IR rats were screened from the Model group. Additionally, western blotting of IR-related proteins in endometrial tissue showed that IRS1 and GLUT-4 expression in the PCOS-IR were decreased (P< 0. 01), suggesting the existence of IR in the endometrial tissue. Compared with the Control group, the PI3K expression level was increased in the PCOS-IR group (P< 0. 05), and the PI3K p110α(P< 0. 01), p-AKT (P< 0. 01), AKT (P> 0. 05) expression levels were decreased in the endometrial tissues, suggesting that it may be related to the down-regulation of PI3K/ AKT pathway-related protein expression in the endometrium. Conclusions Rats with PCOS and IR have characteristic polycystic ovary tissue and abnormal glucose metabolism, and their endometrium is mostly insulin resistant, and may be related to the downregulation of PI3K/ AKT pathway-related protein expression.
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