Paulrayer Antonisamy, Adithan Aravinthan, Lee Jeong Ho, Moon Kwang Hyun, Kim Dae Geun, Im So Yeon, Kang Chang-Won, Kim Nam Soo, Kim Jong-Hoon
College of Veterinary Medicine, BK21PLUS project, Chonbuk National University, 79 Gobong-ro, Iksan-city, Jeollabuk-do 54596, Korea.
Sunchang Reserch Institute of Health and Longevity, Ingye-myeon Indeok-ro, Sunchang-gun, Jeollabuk-do 56015, Korea.
Int J Mol Sci. 2017 Jun 5;18(6):1195. doi: 10.3390/ijms18061195.
(Michx.) Ell. belongs to the Rosaceae family. The purpose of this study is to explore the gastroprotective effect of the hydro-alcoholic extract (AMHAE) against ethanol-induced gastric ulcer in a rat model. Different concentrations (50, 100, and 200 mg/kg) of AMHAE, or 30 mg/kg of omeprazole, significantly inhibited the gastric injury formation. The ethanol-induced ulcer group showed significant increases of malondialdehyde (MDA), myeloperoxidase (MPO), tumor necrosis factor (TNF)-α, nuclear factor-kappaB p65 (NF-κB p65), and monocyte chemoattractant protein (MCP)-1, and decreased activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-px), and interleukin (IL)-4. However, AMHAE (200 mg/kg) pretreatment significantly reversed the altered pathophysiological levels of these biomolecules to near normal stages. The gastroprotective activity of AMHAE was abolished by pretreatment with l-NAME, naloxone, capsazepine, and indomethacin, demonstrating the participation of nitric oxide (NO), opioids, TRPV (vanilloid receptor-related transient receptor potential), and prostaglandins in AMHAE-assisted gastroprotection against ethanol-induced gastric injuries. This gastroprotective effect of AMHAE might be due to the downregulation of TNF-α-based NF-κB, MCP-1 signaling and strong antioxidant properties.
(Michx.) Ell. 属于蔷薇科。本研究的目的是探讨水醇提取物(AMHAE)对大鼠乙醇诱导型胃溃疡的胃保护作用。不同浓度(50、100和200 mg/kg)的AMHAE或30 mg/kg的奥美拉唑可显著抑制胃损伤的形成。乙醇诱导的溃疡组丙二醛(MDA)、髓过氧化物酶(MPO)、肿瘤坏死因子(TNF)-α、核因子-κB p65(NF-κB p65)和单核细胞趋化蛋白(MCP)-1显著增加,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-px)和白细胞介素(IL)-4的活性降低。然而,AMHAE(200 mg/kg)预处理可显著将这些生物分子改变的病理生理水平逆转至接近正常阶段。用L-NAME、纳洛酮、辣椒素和吲哚美辛预处理可消除AMHAE的胃保护活性,表明一氧化氮(NO)、阿片类物质、TRPV(香草酸受体相关瞬时受体电位)和前列腺素参与了AMHAE辅助的对乙醇诱导的胃损伤的胃保护作用。AMHAE的这种胃保护作用可能归因于基于TNF-α的NF-κB、MCP-1信号传导的下调以及强大的抗氧化特性。