Phe-Leu-Ala-Pro 肽通过减轻氧化应激和炎症对 CCl4 引起的急性肝肾损伤的改善作用,ACS Omega

当前位置： X-MOL 学术 › ACS Omega › 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.)

Phe-Leu-Ala-Pro 肽通过减轻氧化应激和炎症对 CCl4 引起的急性肝肾损伤的改善作用
ACS Omega ( IF 3.7 ) Pub Date : 2022-12-02 , DOI: 10.1021/acsomega.2c04851
Shuqi He ₁ , Wei Zhao ₁ , Xiang Chen ₂ , Jie Li ₁ , Leifang Zhang ₁ , Huoxi Jin ₁

Affiliation

急性肝损伤 (ALI) 和急性肾损伤 (AKI) 受抗氧化状态的显着影响。本研究旨在探讨胶原蛋白肽 Phe-Leu-Ala-Pro (FLAP) 对四氯化碳 (CCl ₄ ) 诱导的 ALI 和 AKI 小鼠的保护作用及其机制。结果表明，FLAP有效改善了肝脏质量指数、肾脏质量指数和组织病理学形态。FLAP 治疗显着降低了血清天冬氨酸氨基转移酶 (AST)、丙氨酸氨基转移酶 (ALT)、尿素氮 (BUN) 和肌酐 (CRE) 的水平，但增加了过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD) 和谷胱甘肽过氧化物酶的活性(GSH-Px)。核因子E2相关因子2（Nrf2）、血红素加氧酶-1（HO-1）、pFLAP 治疗后肝脏和肾脏中的β-蛋白激酶 B ( p - AKT) 和p-磷脂酰肌醇-3-激酶 ( p -PI3K) 显着上调。FLAP 下调肝肾组织中白细胞介素 6 (IL-6)、IL-1β、肿瘤坏死因子-α (TNF-α) 和核因子-κ B (NF-κB) 的水平。因此，FLAP 可能通过减弱由 Nrf2/抗反应元件 (ARE) 和 PI3K/AKT/NF-κB 通路介导的氧化应激和炎症，在 ALI 和 AKI 中发挥保护作用。

"点击查看英文标题和摘要"

Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl4 via Attenuation of Oxidative Stress and Inflammation

Acute liver injury (ALI) and acute kidney injury (AKI) are significantly affected by the antioxidant status. In the present study, the protective effect and mechanism of the collagen peptide Phe-Leu-Ala-Pro (FLAP) in mice with ALI and AKI induced by carbon tetrachloride (CCl₄) were examined. The results showed that FLAP effectively improved the liver mass index, the renal mass index, and the histopathological morphology. FLAP treatment significantly decreased the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea nitrogen (BUN), and creatinine (CRE) but increased the activity of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). The protein expression levels of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), p-protein kinase B (p-AKT), and p-phosphatidylinositol-3-kinase (p-PI3K) in the liver and kidneys were significantly up-regulated after FLAP treatment. FLAP down-regulated the levels of interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), and nuclear factor-κ B (NF-κB) in liver and kidney tissues. Thus, FLAP may play a protective role in ALI and AKI by attenuating oxidative stress and inflammation mediated by the Nrf2/anti-response element (ARE) and PI3K/AKT/NF-κB pathways.

更新日期：2022-12-02

点击分享查看原文

点击收藏

公开下载

阅读更多本刊新发论文本刊介绍/投稿指南