当前位置：
X-MOL 学术
›
Mol. Pharmaceutics
›
论文详情
Our official English website, www.x-mol.net, welcomes your
feedback! (Note: you will need to create a separate account there.)
Metformin Protects against LPS-Induced Intestinal Barrier Dysfunction by Activating AMPK Pathway
Molecular Pharmaceutics ( IF 4.5 ) Pub Date : 2018-07-03 00:00:00 , DOI: 10.1021/acs.molpharmaceut.8b00332 Weiche Wu 1 , Sisi Wang 1 , Qing Liu 1 , Tizhong Shan 1 , Yizhen Wang 1
Molecular Pharmaceutics ( IF 4.5 ) Pub Date : 2018-07-03 00:00:00 , DOI: 10.1021/acs.molpharmaceut.8b00332 Weiche Wu 1 , Sisi Wang 1 , Qing Liu 1 , Tizhong Shan 1 , Yizhen Wang 1
Affiliation
|
Metformin not only regulates energy metabolism but also participates in many cellular processes. In this study, we investigated the effect of metformin on lipopolysaccharide (LPS)-induced intestinal barrier damage. We found that LPS treatment decreased the expression of tight junction proteins and caused a proinflammatory response and oxidative stress in the intestine. Interestingly, metformin treatments attenuated LPS-induced intestinal barrier damage, inflammation, and oxidative stress. We found that metformin improved the expression of intestinal tight junction proteins (ZO1, occludin, and Claudin1) that were reduced by LPS stimulation. Moreover, metformin alleviated LPS-induced NF-κB phosphorylation, promoted Nrf2 nuclear translocation, and increased the expression of the antioxidative genes (HO-1 and NQO-1), leading to reduced intestinal ROS content. Mechanistically, we found that metformin protects against LPS-induced intestinal barrier dysfunction by activating AMPK. These results reveal the potential of metformin as an effective therapy for treating intestinal diseases.
中文翻译：
二甲双胍通过激活AMPK途径防止LPS诱导的肠屏障功能障碍
二甲双胍不仅调节能量代谢，而且参与许多细胞过程。在这项研究中，我们调查了二甲双胍对脂多糖（LPS）诱导的肠屏障损伤的影响。我们发现，LPS处理会降低紧密连接蛋白的表达，并引起肠道中的促炎反应和氧化应激。有趣的是，二甲双胍治疗可减轻LPS诱导的肠屏障损伤，炎症和氧化应激。我们发现二甲双胍改善了肠道紧密连接蛋白（ZO1，occludin和Claudin1）的表达，而LPS刺激可降低这种表达。此外，二甲双胍可减轻LPS诱导的NF-κB磷酸化，促进Nrf2核易位，并增加抗氧化基因（HO-1和NQO-1）的表达，导致肠道ROS含量降低。从机理上讲，我们发现二甲双胍可以通过激活AMPK来防止LPS诱导的肠屏障功能障碍。这些结果揭示了二甲双胍作为治疗肠道疾病的有效疗法的潜力。
更新日期：2018-07-03
中文翻译：
二甲双胍通过激活AMPK途径防止LPS诱导的肠屏障功能障碍
二甲双胍不仅调节能量代谢，而且参与许多细胞过程。在这项研究中，我们调查了二甲双胍对脂多糖（LPS）诱导的肠屏障损伤的影响。我们发现，LPS处理会降低紧密连接蛋白的表达，并引起肠道中的促炎反应和氧化应激。有趣的是，二甲双胍治疗可减轻LPS诱导的肠屏障损伤，炎症和氧化应激。我们发现二甲双胍改善了肠道紧密连接蛋白（ZO1，occludin和Claudin1）的表达，而LPS刺激可降低这种表达。此外，二甲双胍可减轻LPS诱导的NF-κB磷酸化，促进Nrf2核易位，并增加抗氧化基因（HO-1和NQO-1）的表达，导致肠道ROS含量降低。从机理上讲，我们发现二甲双胍可以通过激活AMPK来防止LPS诱导的肠屏障功能障碍。这些结果揭示了二甲双胍作为治疗肠道疾病的有效疗法的潜力。
京公网安备 11010802027423号