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罗斯马林酸通过调节NF-κβ通路来保护β细胞免受STZ诱导的细胞损伤

Waseem El-Huneidi^1,2, Shabana Anjum^1,3, Abdul Khader Mohammed¹

¹Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates.

|September 4, 2023

概括

罗斯马林酸 (RA) 在糖尿病实验室模型中保护胰腺β细胞免受损伤. RA 通过调节关键细胞生存和炎症途径来保持胰岛素分泌和β细胞功能.

科学领域:

生物化学生化学
细胞生物学细胞生物学
药理学药理学是指药理学的学科.

背景情况:

罗斯马林酸 (RA) 是一种天然的化合物,具有已知的抗氧化和抗炎作用.
之前的研究表明,RA可能具有降血糖效应,但根本机制尚不清楚.

研究的目的:

用INS-1细胞在体外模型中研究罗斯马林酸 (RA) 的抗糖尿病作用和潜在机制.
为了确定RA是否可以保护胰腺β细胞免受链毒素 (STZ) 诱导的损伤.

主要方法:

一个体外糖尿病模型是通过用链毒素 (STZ) 治疗INS-1细胞而创建的.
细胞被先处理了不同度的罗斯马林酸 (RA) (1和2.5微米).
评估了细胞活力,葡萄糖刺激胰岛素分泌 (GSIS),葡萄糖吸收,脂质过氧化,活性氧物种 (ROS),亡和蛋白质表达 (Bcl-2,NF-κB,IL-1β,PARP).

主要成果:

在INS-1细胞中,STZ诱导的损伤导致细胞活力,胰岛素分泌,胰岛素含量和葡萄糖吸收降低,同时增加脂质过氧化 (MDA) 和ROS水平.
在RA前期治疗保护了INS-1细胞,维持了它们的功能和形态,防止STZ引起的损伤.
关节炎治疗可提高Bcl-2蛋白表达的调节,同时降低NF-κB,IL-1β和PARP表达的调节.

结论:

罗斯马林酸 (RA) 在实验室中表现出对STZ诱导的胰腺β细胞损伤的保护作用.
通过调节NF-κB和Bcl-2信号通路,RA可以保持β细胞的功能和活力.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.Bcl-2 的使用方法.糖尿病糖尿病糖尿病一个INS-1细胞.在 NF-κBB 中.罗斯马林酸是一种酸.这就是STZ STZ.

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