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伊根明木可以通过调节Kir4.1/AQP4轴来抑制糖尿病黄斑胀:基于网络药理学的研究

Longrong Huang¹, Xinyi Guo¹, Qi Hu¹

¹Department of Ophthalmology, The First Affiliated Hospital of Hunan University of Chinese Medicine Changsha 431000, Hunan, China.

American journal of translational research

|December 11, 2023

概括

伊根明慕 (YGMMD) 通过调节水素4 (AQP4) 和通过ERK1/2-PI3K-AKT通路向内纠正通道亚型4.1 (Kir4.1) 表达,有效地治疗糖尿病黄斑 (DME). 这恢复了视网膜液平衡,并缓解了DME症状.

科学领域:

眼科医生眼科眼科
药理学药理学是指药理学的学科.
糖尿病学糖尿病学

背景情况:

糖尿病黄斑 (DME) 是糖尿病患者视力丧失的主要原因.
目前对DME的治疗有局限性,需要新的治疗方法.

研究的目的:

研究Yigan Mingmu Decoction (YGMMD) 的治疗潜力和潜在机制,以预防和治疗糖尿病黄斑 (DME).

主要方法:

网络药理学被用来识别YGMMD的生物活性化合物和标.
在体内研究中使用了用YGMMD治疗的Sprague Dawley大鼠来评估其对血糖,体重和视网膜病理的影响.
西方涂抹,免疫光和免疫组织化学被用来分析关键蛋白质表达,包括AQP4,Kir4.1,p-ERK1/2和p-AKT.

主要成果:

网络药理学和分子对接表示YGMMD调节DME中的AQP4/Kir4.1.
在老鼠中,YGMMD显示出显著的低血糖效应和减少视网膜.
治疗YGMMD调节了AQP4,Kir4.1,p-ERK1/2和p-AKT的表达,这表明它在ERK1/2-PI3K-AKT通路中发挥了作用.

结论:

YGMMD通过抑制p-ERK1/2和增强p-AKT来缓解DME,这会降低AQP4的调节,并提高Kir4.1.1.的调节.
这种机制恢复了视网膜液清除系统,为DME提供了潜在的治疗方法.

关键词:

糖尿病视网膜病变 - 糖尿病视网膜病变实验验证实验验验证实验验验证实验验验证实验验验验证实验验验证实验验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验验证实验验证实验验验证实验验验证实验验验证实验验验验证实验验验验验证分子对接的分子对接.水平衡水平衡水平衡水平衡

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