科尔克胡尼亚根片通过通过PTEN/PI3K/AKT通路调节上皮质-介质细胞过渡来改善糖尿病病
Donghong Ma1,2, Jiao Zhang1, Lu Du1
1Department of Nephrology, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan Province, China.
Frontiers in pharmacology
|August 12, 2024
概括
科尔库胡尼亚根药片 (CRT) 通过减少蛋白尿和抑制上皮-介质细胞过渡 (EMT) 来有效治疗糖尿病病 (DKD). 通过对抑制PI3K/AKT通路的PTEN进行上调,CRT的作用为DKD提供了新的治疗见解.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 药理学 药理学是指药理学的学科.
- 分子生物学分子生物学
背景情况:
- 糖尿病病 (DKD) 是糖尿病的严重并发症,可能导致末期病.
- 科尔库胡尼亚根片 (CRT) 显示在DKD治疗中具有前景,但其疗效和机制需要进一步研究.
研究的目的:
- 评估CRT在DKD患者的临床疗效.
- 研究CRT在细胞中对高葡萄糖诱导的上皮层-介质细胞过渡 (EMT) 的体外影响.
- 阐明CRT作用背后的分子机制,重点关注PTEN/PI3K/AKT通路.
主要方法:
- 一个为期3个月的随机对照试验,涉及61名DKD患者,比较CRT加标准治疗与单独标准治疗.
- 在体外实验中使用暴露于高葡萄糖 (HG) 的人类管状上皮细胞 (HK-2).
- 蛋白尿的评估,治疗疗效,不良事件和分子变化 (α-SMA,E-cadherin,PTEN,PI3K/AKT通路).
主要成果:
- CRT显著改善了蛋白尿,并增加了DKD患者的有效治疗率,而不会增加不良事件.
- 在HK-2细胞中,CRT逆转了HG诱导的EMT,降低了α-SMA并增加了E-cadherin的表达.
- CRT上调了PTEN,并抑制了PI3K/AKT通路,CRT和LY29400结合进一步增强了PTEN的表达.
结论:
- 在DKD患者中,CRT有效改善蛋白尿症.
- 在细胞中,CRT改善了HG诱导的EMT,可能是通过PTEN上调和PI3K/AKT通路抑制.
- CRT为DKD提供了一个有前途的治疗选择,其潜在的机制涉及PTEN/PI3K/AKT信号通路.
更多相关视频
08:15Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
Published on: May 10, 2024
530
10:37Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
108
相关概念视频
01:23Dipeptidyl Peptidase 4 Inhibitors
180
Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
180
01:22PI3K/mTOR/AKT Signaling Pathway
3.5K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.5K