脂质过氧化
髓过氧化物酶
超氧化物歧化酶
白三烯B4
化学
药理学
谷胱甘肽
前列腺素E2
谷胱甘肽过氧化物酶
白细胞介素
丙二醛
内科学
抗氧化剂
肿瘤坏死因子α
内分泌学
细胞因子
医学
生物化学
炎症
酶
作者
Paulrayer Antonisamy,Mariadhas Valan Arasu,Muniappan Dhanasekaran,Ki Choon Choi,Adithan Aravinthan,Nam Soo Kim,Chang‐Won Kang,Jong‐Hoon Kim
出处
期刊:Food & Function
[The Royal Society of Chemistry]
日期:2016-01-01
卷期号:7 (1): 398-408
被引量:50
摘要
The present study was undertaken to explore gastroprotective effects of trigonelline (TRG) and to determine the potential mechanisms involved in this action. In order to evaluate the gastroprotective efficiency of TRG, an indomethacin-induced ulcer model has been applied. Antioxidants, cytokines, adhesion markers and apoptosis levels have been analyzed for the biochemical mechanism involved in TRG activity. TRG (45 mg kg(-1)) pretreated rats significantly inhibited gastric lesions by 81.71%. Indomethacin administration raises the levels of leukotriene B4 (LTB4), lipid peroxidation and myeloperoxidase (MPO) with the significant declines of prostaglandin E2 (PGE2), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-px) levels. Conversely, TRG (45 mg kg(-1)) pretreated animals showed significant rises in PGE2 and antioxidant levels along with substantial reductions in LTB4, lipid peroxidation and MPO levels. Indomethacin-induced rats also exhibited considerable increases of pro-inflammatory cytokines including interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) levels and decreases of anti-inflammatory cytokines such as interleukin-10 (IL-10) and interleukin-4 (IL-4), but these imbalances were normalized through treatment of TRG. The protective activity of TRG against indomethacin-induced gastric ulcer has been ascribed to three important mechanisms: (1) anti-inflammatory; (2) antioxidant; (3) anti-apoptotic pathways.
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