药理学
谷胱甘肽
血红素加氧酶
化学
小檗碱
吲哚美辛
超氧化物歧化酶
p38丝裂原活化蛋白激酶
免疫印迹
髓过氧化物酶
肿瘤坏死因子α
蛋白激酶A
前列腺素E2
环氧合酶
氧化应激
激酶
生物化学
内分泌学
内科学
医学
炎症
血红素
酶
基因
前列腺素内过氧化物合酶
作者
Chaodan Luo,Hanbin Chen,Yongfu Wang,G. David Lin,Cailan Li,Lihua Tan,Zi‐Ren Su,Xiaoping Lai,Jianhui Xie,Hui Zeng
出处
期刊:Life Sciences
[Elsevier]
日期:2018-01-01
卷期号:193: 47-56
被引量:36
标识
DOI:10.1016/j.lfs.2017.12.004
摘要
The aim of this study was to comparatively investigate the potential gastroprotective effect and underlying mechanisms of coptisine free base (CFB, 8-hydroxy-7, 8-dihydrocoptisine), berberine and lansoprazole against indomethacin-induced gastric ulcer in rats. CFB (10, 20 and 40 mg/kg), berberine (20 mg/kg) and lansoprazole (30 mg/kg) were orally administrated to rats prior to indometacin ingestion, and gastric lesions were evaluated macroscopically and histologically, and further analyzed by ELISA, qRT-PCR and Western blot. CFB exerted comparable or superior gastroprotective effect to berberine in protecting against indomethacin-induced gastric injury. CFB pretreatment significantly enhanced the levels of superoxide dismutase (SOD) and glutathione (GSH), and markedly decreased the malonaldehyde (MDA) content. CFB administration effectively suppressed the levels of myeloperoxidase (MPO), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and angiotensin II (Ang II). Besides, CFB substantially up-regulated the mRNA expressions of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and promoted gastric mucosal prostaglandin E2 level (PGE2). Furthermore, CFB pretreatment remarkably increased the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) from cytosol into the nucleus, and the expression of heme oxygenase-1 (HO-1), while significantly decreased the expression of mitogen activated protein Kinase Kinase 6 (MKK6) and translocation of p38 mitogen-activated protein kinase (p38 MAPK). This was the first investigation reporting the anti-ulcer effect of protoberberine alkaloid free base on in vivo rodent model. The gastroprotective mechanism of CFB might involve favorable regulation of antioxidant and anti-inflammatory status mediated, at least partially, by the Nrf2 signaling pathway and p38 MAPK translocation.
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