人参皂苷对细胞焦亡的干预作用及在糖尿病肾病中的治疗潜力
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篇名: 人参皂苷对细胞焦亡的干预作用及在糖尿病肾病中的治疗潜力
TITLE: Interventional effects of ginsenoside in pyroptosis and its potential for the treatment of diabetic nephropathy
摘要: 糖尿病肾病(DN)是糖尿病患者常见的并发症之一,是导致终末期肾病的主要原因。细胞焦亡是一种程序性细胞死亡方式,在DN的发生发展中起着重要作用。足细胞、肾小球内皮细胞和肾小管上皮细胞的焦亡会导致肾损伤和功能障碍,从而加速DN的进展。研究表明,多种人参皂苷在抑制细胞焦亡相关通路方面具有潜力,从而为DN治疗提供了新的思路。其中,人参皂苷化合物K、Rg5、Rg1、Rh2和Rb1等可通过调节核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体3炎症小体通路中的关键蛋白(如胱天蛋白酶1、核因子κB、焦孔素D蛋白氮端片段、白细胞介素1β和白细胞介素18等),抑制炎症反应和细胞焦亡,从而发挥对DN的干预作用。然而,目前大部分研究集中于动物模型,尚需进一步的临床试验来验证人参皂苷在人体中的疗效和安全性;同时,还需深入探索不同个体对人参皂苷的反应差异,以及人参皂苷针对细胞焦亡途径的精细调节机制,以优化治疗效果并减少潜在的副作用。
ABSTRACT: Diabetic nephropathy (DN) is a common complication of diabetes and the leading cause of end-stage renal disease. Pyroptosis is a mode of programmed cell death that plays an important role in the development of DN. Pyroptosis of podocytes, glomerular endothelial cells and tubular epithelial cells leads to renal injury and dysfunction, accelerating the progression of DN. In recent years, studies have shown that a variety of ginsenosides have the potential to inhibit pyroptosis-related pathways, providing new ideas for DN treatment. Among them, ginsenoside compound K, ginsenoside Rg5, ginsenoside Rg1, ginsenoside Rh2 and ginsenoside Rb1 exert a protective effect against DN by regulating nucleotide-binding domain-rich repeat and pyrin domain- containing protein 3 inflammatory vesicle pathway, such as caspase-1, nuclear factor-κB, gasdermin D-N, interleukin-1β (IL-1β) and IL-18, thereby inhibiting inflammation and cellular pyroptosis. However, most current studies have focused on animal models, and further clinical trials are needed to verify the efficacy and safety of ginsenosides in humans. In addition, future studies need to explore the differences in response to ginsenosides in different individuals and the fine-tuning mechanism of ginsenosides against the cellular pyroptosis pathway to optimize therapeutic efficacy and reduce potential side effects.
期刊: 2024年第35卷第24期
作者: 韦缘;周恩超
AUTHORS: WEI Yuan,ZHOU Enchao
关键字: 人参皂苷;糖尿病肾病;细胞焦亡;作用机制;炎症反应
KEYWORDS:
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