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荜茇水醇提取物对雨蛙肽诱导的胰腺炎症的调节作用。

Modulation of cerulein-induced pancreatic inflammation by hydroalcoholic extract of curry leaf (Murraya koenigii).

机构信息

Department of Regulatory Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, Telangana State, India.

出版信息

Phytother Res. 2019 May;33(5):1510-1525. doi: 10.1002/ptr.6344. Epub 2019 Mar 18.

Abstract

This study was performed to study the in vitro and in vivo efficacy of hydroalcoholic extract of curry leaf (CLE) rich in carbazole alkaloids, against LPS-induced inflammation in Raw 264.7 macrophages and cerulein-induced acute pancreatitis, respectively. CLE was characterized by Fourier-transform infrared (FTIR) and liquid chromatography-mass spectrometry. Raw 264.7 cells were stimulated with LPS (2 μg/ml) and treated with CLE. The animals were treated with two doses of CLE (100 and 300 mg/kg). Plasma biochemistry, tissue lipid peroxidation, cytokines, and histological examination were evaluated. CLE was found to decently scavenge the activity of DPPH radical. It dose dependently suppressed nitrite production and oxidative stress in macrophages. CLE alleviated LPS-induced inflammation in macrophages as evident from the results of various inflammatory cytokines (IL-1β, IL-6, and TNF-α). In vivo, CLE reduced cerulein-induced pancreatic edema. CLE significantly abrogated the cerulein-induced lipid peroxidation, nitrite, MPO, and GSH levels. The inflammatory cytokines and p65-NFκB activity were significantly reduced by CLE. Mechanistically, CLE reduced the expression of NT, MPO, IL-1β, ICAM-1, and COX-2, and increased the expression of Nrf2. It reduced distant organ damage markers as well. We report for the first time that CLE holds substantial potential for the prevention of acute pancreatitis.

摘要

本研究旨在分别研究富含咔唑生物碱的咖喱叶水醇提取物(CLE)在体外和体内对 LPS 诱导的 Raw 264.7 巨噬细胞炎症和 Cerulein 诱导的急性胰腺炎的疗效。CLE 通过傅里叶变换红外(FTIR)和液相色谱-质谱进行了表征。用 LPS(2 μg/ml)刺激 Raw 264.7 细胞并用 CLE 处理。用两种剂量的 CLE(100 和 300 mg/kg)对动物进行治疗。评估了血浆生化、组织脂质过氧化、细胞因子和组织学检查。CLE 被发现能够相当好地清除 DPPH 自由基的活性。它可剂量依赖性地抑制巨噬细胞中亚硝酸盐的产生和氧化应激。CLE 减轻了 LPS 诱导的巨噬细胞炎症,这从各种炎症细胞因子(IL-1β、IL-6 和 TNF-α)的结果中可以明显看出。在体内,CLE 减轻了 Cerulein 诱导的胰腺水肿。CLE 显著减轻了 Cerulein 诱导的脂质过氧化、亚硝酸盐、MPO 和 GSH 水平。CLE 还降低了炎症细胞因子和 p65-NFκB 的活性。从机制上讲,CLE 降低了 NT、MPO、IL-1β、ICAM-1 和 COX-2 的表达,并增加了 Nrf2 的表达。它还降低了远处器官损伤标志物的水平。我们首次报道 CLE 具有预防急性胰腺炎的巨大潜力。

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