Zeren Sezgin, Bayhan Zulfu, Kocak Fatma Emel, Kocak Cengiz, Akcılar Raziye, Bayat Zeynep, Simsek Hasan, Duzgun Sukru Aydin
Faculty of Medicine, Department of General Surgery, Dumlupinar University, Kutahya, Turkey.
Faculty of Medicine, Department of General Surgery, Dumlupinar University, Kutahya, Turkey.
J Surg Res. 2016 Jun 15;203(2):348-59. doi: 10.1016/j.jss.2016.03.027. Epub 2016 Mar 24.
Nonsteroidal anti-inflammatory drugs (NSAIDs) commonly cause gastric ulcers (GUs). We investigated the effects of sulforaphane (SF) and thymoquinone (TQ) in rats with acetylsalicylic acid (ASA)-induced GUs.
Thirty-five male Wistar-Albino rats were divided into five groups: control; ASA; ASA with vehicle; ASA + SF; and ASA + TQ. Compounds were administered by oral gavage before GU induction. GUs were induced by intragastric administration of ASA. Four hours after GU induction, rats were killed and stomachs excised. Total oxidant status, total antioxidant status, total thiol, nitric oxide, asymmetric dimethylarginine, tumor necrosis factor-alpha levels, superoxide dismutase activity, and glutathione peroxidase activity in tissue were measured. Messenger RNA expression of dimethylarginine dimethylaminohydrolases, heme oxygenase-1 (HO-1), nuclear factor erythroid 2-related factor 2, and nuclear factor kappa-light-chain-enhancer of activated B cells were analyzed. Renal tissues were evaluated by histopathologic and immunohistochemical means.
SF and TQ reduced GU indices, apoptosis, total oxidant status, asymmetric dimethylarginine, and tumor necrosis factor-alpha levels, nuclear factor kappa-light-chain-enhancer of activated B cells, and inducible nitric oxide synthase expressions (P < 0.001, P = 0.001). Both examined compounds increased superoxide dismutase activity, glutathione peroxidase activity, total antioxidant status, total thiol, nitric oxide levels, endothelial nitric oxide synthase, dimethylarginine dimethylaminohydrolases, HO-1, nuclear factor erythroid 2-related factor 2, and HO-1 expressions (P < 0.001).
These results suggest that pretreatment with SF or TQ can reduce ASA-induced GUs via anti-inflammatory, antioxidant, and antiapoptotic effects. These compounds may be useful therapeutic strategies to prevent the gastrointestinal adverse effects that limit nonsteroidal anti-inflammatory drugs use.
非甾体抗炎药（NSAIDs）常导致胃溃疡（GUs）。我们研究了萝卜硫素（SF）和百里醌（TQ）对乙酰水杨酸（ASA）诱导的大鼠胃溃疡的影响。
35只雄性Wistar - 白化大鼠分为五组：对照组；ASA组；ASA加赋形剂组；ASA + SF组；ASA + TQ组。在诱导胃溃疡前通过口服灌胃给予化合物。通过胃内给予ASA诱导胃溃疡。诱导胃溃疡4小时后，处死大鼠并切除胃。测量组织中的总氧化剂状态、总抗氧化剂状态、总硫醇、一氧化氮、不对称二甲基精氨酸、肿瘤坏死因子 - α水平、超氧化物歧化酶活性和谷胱甘肽过氧化物酶活性。分析二甲基精氨酸二甲胺水解酶、血红素加氧酶 - 1（HO - 1）、核因子红细胞2相关因子2和活化B细胞的核因子κ轻链增强子的信使核糖核酸表达。通过组织病理学和免疫组织化学方法评估肾脏组织。
SF和TQ降低了胃溃疡指数、细胞凋亡、总氧化剂状态、不对称二甲基精氨酸和肿瘤坏死因子 - α水平、活化B细胞的核因子κ轻链增强子以及诱导型一氧化氮合酶表达（P < 0.001，P = 0.001）。两种受试化合物均增加了超氧化物歧化酶活性、谷胱甘肽过氧化物酶活性、总抗氧化剂状态、总硫醇、一氧化氮水平、内皮型一氧化氮合酶、二甲基精氨酸二甲胺水解酶、HO - 1、核因子红细胞2相关因子2和HO - 1表达（P < 0.001）。
这些结果表明，SF或TQ预处理可通过抗炎、抗氧化和抗凋亡作用减少ASA诱导的胃溃疡。这些化合物可能是预防限制非甾体抗炎药使用的胃肠道不良反应的有用治疗策略。
