| 引用本文: | 宾慧莹,唐彦慧,唐琪,梁日雄,曾雪怡,林丽霞,韦海澄,覃柳,胡品章,凌宇.2型糖尿病视网膜病变患者外周血及高糖诱导的视网膜微血管内皮细胞中PIK3IP1的表达分析[J].中国临床新医学,,():-. |
| binhuiying.2型糖尿病视网膜病变患者外周血及高糖诱导的视网膜微血管内皮细胞中PIK3IP1的表达分析[J].中国临床新医学,,():-. |
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| 2型糖尿病视网膜病变患者外周血及高糖诱导的视网膜微血管内皮细胞中PIK3IP1的表达分析 |
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宾慧莹,唐彦慧,唐琪,梁日雄,曾雪怡,林丽霞,韦海澄,覃柳,胡品章,凌宇
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1.南宁市第一人民医院;2.南宁市卫生健康委员会
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| 摘要: |
| 目的 分析2型糖尿病视网膜病变患者外周血及高糖诱导的视网膜微血管内皮细胞中PIK3IP1的表达水平,为探索PIK3IP1在DR发病过程中的潜在作用提供初步思路。方法 选取2023年9月至2024年12月南宁市第一人民医院眼科及内分泌科收治的92例T2DM患者,根据眼底检查结果将患者分为正常眼底组(T2DM组,45例)和糖尿病视网膜病变组(DR组,47例)。选取本院同期体检健康者作为对照组(48例)。于入组后次日清晨采集所有研究对象空腹外周静脉血用于后续实验。使用实时荧光定量PCR(RT-qPCR)和蛋白质印迹法(WB)分别检测外周血中PIK3IP1 mRNA和蛋白水平。采用Spearman秩相关或Pearson相关分析 PIK3IP1水平与临床变量的相关性。采用多元线性回归分析PIK3IP1水平的影响因素。采用CCK-8法筛选构建体外人视网膜微血管内皮细胞(HRMECs)高糖损伤模型。通过 RT-qPCR 和WB 检测对照组(5.5 mmol/L, NG组)与高糖组(HG组)细胞中 PIK3IP1 mRNA 和蛋白水平,检测与PI3K/AKT信号通路激活有关的p-AKT、AKT 蛋白水平,计算p-AKT/AKT蛋白水平。结果 DR组PIK3IP1 mRNA和蛋白表达水平显著高于对照组和T2DM组(P<0.05)。PIK3IP1水平与BMI、WBC、FPG呈正相关(P<0.05)。多元线性回归分析结果显示,FPG是PIK3IP1水平的影响因素(P<0.05)。与NG组比较,HG组细胞中PIK3IP1 mRNA和蛋白水平升高(P<0.05),p-AKT、p-AKT/AKT蛋白水平降低(P<0.05)。结论 PIK3IP1在DR患者外周血和体外HRMECs高糖损伤细胞中表达上调,FPG是影响PIK3IP1水平的影响因素。 |
| 关键词: 糖尿病视网膜病变 磷脂酰肌醇-3激酶相互作用蛋白1 人视网膜微血管内皮细胞 PI3K/AKT 信号通路 |
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| 基金项目:广西自然科学基金面上项目(编号:2023GXNSFAA026071) |
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| Expression analysis of PIK3IP1 in peripheral blood of patients with type 2 diabetic retinopathy and in retinal microvascular endothelial cells induced by high glucose |
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binhuiying1,2,3
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1.The First People'2.'3.s Hospital of Nanning
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| Abstract: |
| Objective To analyze the expression levels of PIK3IP1 in peripheral blood of patients with type 2 diabetic retinopathy and in high glucose-treated human retinal microvascular endothelial cells, and to provide preliminary insights into the potential role of PIK3IP1 in the pathogenesis of DR. Methods (1) A total of 92 patients with type 2 diabetes mellitus (T2DM) admitted to the Ophthalmology and Endocrinology Department of the First People's Hospital of Nanning from September 2023 to December 2024 were selected. According to the results of fundus examination, the patients were divided into the normal fundus group (T2DM group, 45 cases) and the diabetic retinopathy group (DR Group, 47 cases). Forty-eight healthy people who underwent physical examination in our hospital during the same period were selected as the control group. Fasting peripheral venous blood was collected from all subjects in the morning of the next day after enrollment for subsequent experiments. Real-time quantitative PCR (RT-qPCR) and Western blotting (WB) were used to detect the mRNA and protein levels of PIK3IP1 in peripheral blood, respectively. Spearman rank correlation or Pearson correlation was used to analyze the correlation between PIK3IP1 levels and clinical variables. Multivariate linear regression analysis was used to analyze the influencing factors of PIK3IP1 level. CCK-8 method was used to screen and construct high glucose injury model of human retinal microvascular endothelial cells (HRMECs) in vitro. The mRNA and protein levels of PIK3IP1 in the control group (5.5 mmol/L, NG group) and the high glucose group (HG group) were detected by RT-qPCR and WB. The protein levels of p-AKT and AKT related to the activation of PI3K/AKT signaling pathway were detected, and the protein level of p-AKT/AKT was calculated. Results The expression levels of PIK3IP1 mRNA and protein in the DR Group were significantly higher than those in the control group and the T2DM group (P < 0.05). PIK3IP1 level was positively correlated with BMI, WBC and FPG (P < 0.05). Multiple linear regression analysis showed that FPG was the influencing factor of PIK3IP1 level (P < 0.05). Compared with NG group, the mRNA and protein levels of PIK3IP1 in HG group were increased (P < 0.05), and the protein levels of p-Akt and p-Akt /AKT were decreased (P < 0.05). Conclusion The expression of PIK3IP1 is up-regulated in peripheral blood of DR Patients and in high glucose-damaged cells of HRMECs in vitro. FPG is an influencing factor for PIK3IP1 level. |
| Key words: diabetic retinopathy phosphoinositide-3 kinase interacting protein 1 human retinal microvascular endothelial cells PI3K/AKT signaling pathway |