This study investigated the effect of carvedilol on aspirin-induced gastric damage. Male Wistar rats were divided into three groups. Control rats received the vehicle, while the aspirin group received aspirin (200 mg/kg) orally for 4 days. Rats of aspirin + carvedilol group were administered aspirin along with carvedilol (5 mg/kg; intraperitoneal) for 4 days. Animals were euthanized at the end of the treatment period, and gastric tissues were collected to perform histopathological and mechanistic studies. The results revealed that aspirin administration induced gastric ulcer as there were remarkable histopathological lesions in the form of marked necrosis, inflammation, hemorrhage, edema, and dysplastic changes. Lipid peroxidative markers such as malondialdehyde, 4-hydroxynonenal, and protein carbonyl were significantly elevated in the aspirin group. This was concurrent with a significant amelioration of antioxidants such as reduced glutathione, superoxide dismutase, and catalase. Furthermore, aspirin increased the immunoexpression of cyclooxygenase (COX) 2 and nuclear factor kappa-B (NF-κB). Aspirin induced elevation in the inflammatory cytokines such as tumor necrosis factor-α, interleukin-6, and interleukin-1β. Aspirin enhanced the immunoexpression of inducible nitric oxide synthetase (iNOS) and increased the level of nitrite/nitrate in gastric tissue. On the other hand, carvedilol treatment reversed all these pathological changes. Carvedilol succeeded to enhance antioxidants in gastric tissue, attenuated lipid peroxidative parameters, and suppressed the release of inflammatory mediators. It attenuated the immunoexpression of COX-2, NF-κB, and iNOS. Collectively, carvedilol has a gastro-protective effect that could be attributed to its antioxidative and anti-inflammatory properties, which modulate NF-κB/COX-2/iNOS pathways.

中文翻译：

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卡维地洛可以预防阿司匹林引起的大鼠胃部损伤。

这项研究调查了卡维地洛对阿司匹林引起的胃损害的影响。将雄性Wistar大鼠分成三组。对照组大鼠接受媒介物，而阿司匹林组口服阿司匹林（200 mg / kg）4天。阿司匹林+卡维地洛组的大鼠被给予阿司匹林和卡维地洛（5 mg / kg；腹膜内）4天。在治疗期结束时对动物实施安乐死，并收集胃组织以进行组织病理学和力学研究。结果显示，服用阿司匹林可引起胃溃疡，因为存在明显的组织病理学损害，表现为明显的坏死，炎症，出血，水肿和增生异常改变。脂质过氧化标记，例如丙二醛，4-羟基壬烯醛，阿司匹林组蛋白和羰基蛋白显着升高。这与抗氧化剂的显着改善同时进行，例​​如减少的谷胱甘肽，超氧化物歧化酶和过氧化氢酶。此外，阿司匹林提高了环氧合酶（COX）2和核因子κB（NF-κB）的免疫表达。阿司匹林诱导炎性细胞因子如肿瘤坏死因子-α，白介素-6和白介素-1β升高。阿司匹林增强了诱导型一氧化氮合成酶（iNOS）的免疫表达，并提高了胃组织中亚硝酸盐/硝酸盐的水平。另一方面，卡维地洛治疗可逆转所有这些病理变化。卡维地洛成功地增强了胃组织中的抗氧化剂，减弱了脂质过氧化参数，并抑制了炎症介质的释放。它减弱了COX-2，NF-κB和iNOS的免疫表达。总的来说，卡维地洛具有保护胃的作用，这归因于其抗氧化和抗炎特性，可调节NF-κB/ COX-2 / iNOS途径。