Antonisamy Paulrayer, Arasu Mariadhas Valan, Dhanasekaran Muniappan, Choi Ki Choon, Aravinthan Adithan, Kim Nam Soo, Kang Chang-Won, Kim Jong-Hoon
College of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University, 54596 79 Gobong-ro, Iksan-city, Jeollabuk-Do, Republic of Korea.
Department of Botany and Microbiology, Addiriyah Chair for Environmental Studies, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia.
Food Funct. 2016 Jan;7(1):398-408. doi: 10.1039/c5fo00403a.
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.
本研究旨在探讨胡芦巴碱（TRG）的胃保护作用，并确定其作用的潜在机制。为了评估TRG的胃保护效率，采用了吲哚美辛诱导的溃疡模型。分析了抗氧化剂、细胞因子、黏附标志物和细胞凋亡水平，以探讨TRG活性的生化机制。TRG（45mg/kg）预处理的大鼠胃损伤显著抑制了81.71%。吲哚美辛给药使白三烯B4（LTB4）、脂质过氧化和髓过氧化物酶（MPO）水平升高，同时前列腺素E2（PGE2）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSH-px）水平显著下降。相反，TRG（45mg/kg）预处理的动物PGE2和抗氧化剂水平显著升高，同时LTB4、脂质过氧化和MPO水平大幅降低。吲哚美辛诱导的大鼠促炎细胞因子包括白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）水平也显著升高，抗炎细胞因子如白细胞介素-10（IL-10）和白细胞介素-4（IL-4）水平降低，但通过TRG治疗这些失衡得以恢复正常。TRG对吲哚美辛诱导的胃溃疡的保护作用归因于三个重要机制：（1）抗炎；（2）抗氧化；（3）抗凋亡途径。
