Akmal Muhamad Nurul, Abdel Aziz Ibrahim, Nur Azlina Mohd Fahami
Department of Pharmacology, Faculty of Medicine, UKM Medical Centre, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia.
Department of Pharmacology and Toxicology, Faculty of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia.
Front Pharmacol. 2023 Jan 12;13:971443. doi: 10.3389/fphar.2022.971443. eCollection 2022.
This study investigated the gastroprotective effect of (PS) on stress-induced gastric ulcers in rats by measuring its effect on oxidative stress, gastric mucosal nitric oxide (NO), and inflammatory biomarkers. Twenty-eight male Wistar rats were randomly divided into four groups; two control groups (non-stress and stress) and two treated groups supplemented with either methanolic PS extract (500 mg/kg body weight) or omeprazole (OMZ; 20 mg/kg) orally. After 28 days of treatment, the stress control, PS, and OMZ groups were subjected to water-immersion restrain stress (WIRS) for 3.5 h. Gastric tissue malondialdehyde (MDA), NO, superoxide dismutase (SOD), inducible NO synthase (iNOS), SOD mRNA, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were measured. WIRS significantly increased gastric MDA, NO, and pro-inflammatory cytokine levels compared to the non-stressed control group. PS and omeprazole supplementation significantly reduced WIRS-exposure-induced gastric ulcers and MDA, iNOS, and IL-1β levels. However, only PS reduced NO, TNF-α, and IL-6 levels, which were upregulated in this ulcer model. In conclusion, the gastroprotection afforded by PS is possibly mediated by gastric mucosal NO normalization through reduced iNOS expression and attenuation of inflammatory cytokines. PS showed a greater protective effect than omeprazole in reducing gastric lesions and NO, TNF-α, and IL-6 levels, and iNOS expression.
本研究通过测量其对氧化应激、胃黏膜一氧化氮(NO)和炎症生物标志物的影响,探讨了[具体物质](PS)对大鼠应激性胃溃疡的胃保护作用。28只雄性Wistar大鼠随机分为四组;两个对照组(非应激组和应激组)和两个治疗组,分别口服补充甲醇提取物PS(500mg/kg体重)或奥美拉唑(OMZ;20mg/kg)。治疗28天后,应激对照组、PS组和OMZ组接受3.5小时的水浸束缚应激(WIRS)。检测胃组织丙二醛(MDA)、NO、超氧化物歧化酶(SOD)、诱导型NO合酶(iNOS)、SOD mRNA、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和IL-6水平。与非应激对照组相比,WIRS显著增加了胃MDA、NO和促炎细胞因子水平。补充PS和奥美拉唑显著减少了WIRS暴露诱导的胃溃疡以及MDA、iNOS和IL-1β水平。然而,只有PS降低了该溃疡模型中上调的NO、TNF-α和IL-6水平。总之,PS提供的胃保护作用可能是通过降低iNOS表达和减轻炎症细胞因子来使胃黏膜NO正常化介导的。在减少胃损伤、NO、TNF-α和IL-6水平以及iNOS表达方面,PS显示出比奥美拉唑更强的保护作用。