Department of Physiology and Pharmacology, Biomedical Institute of Brazilian Semi-arid, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.
Chem Biol Interact. 2010 Jan 5;183(1):264-9. doi: 10.1016/j.cbi.2009.10.008.
Cashew nut-shell liquid and the contained anacardic acids (AAs) have been shown to possess antioxidant, lipoxygenase inhibitory, anti-Helicobacter pylori and antitumor properties. Despite these known effects, hitherto there were no published reports on their likely gastroprotective effects. The present study was designed to verify whether AAs afford gastroprotection against the ethanol-induced gastric damage and to examine the underlying mechanism(s). Gastric damage was induced by intragastric administration of 0.2mL of ethanol (96%). Mice in groups were pretreated orally with AAs (10, 30 and 100mg/kg), misoprostol (50 microg/kg), or vehicle (2% Tween 80 in saline, 10mL/kg), 45min before ethanol administration. They were sacrificed 30min later, the stomachs excised, and the mucosal lesion area (mm(2)) measured by planimetry. Gastroprotection was assessed in relation to inhibition of gastric lesion area. To study the gastroprotective mechanism(s), its relations to capsaicin-sensitive fibers, endogenous prostaglandins, nitric oxide and ATP-sensitive potassium channels were analysed. Treatments effects on ethanol-associated oxidative stress markers GSH, MDA, catalase, SOD, and total nitrate/nitrite levels as an index of NO were measured in gastric tissue. Besides, the effects of AAs on gastric secretory volume and total acidity were analysed in 4-h pylorus-ligated rat. AAs afforded a dose-related gastroprotection against the ethanol damage and further prevented the ethanol-induced changes in the levels of GSH, MDA, catalase, SOD and nitrate/nitrite. However, they failed to modify the gastric secretion or the total acidity. It was observed that the gastroprotection by AAs was greatly reduced in animals pretreated with capsazepine, indomethacin, l-NAME or glibenclamide. These results suggest that AAs afford gastroprotection principally through an antioxidant mechanism. Other complementary mechanisms include the activation of capsaicin-sensitive gastric afferents, stimulation of endogenous prostaglandins and nitric oxide, and opening of K(+)(ATP) channels. These combined effects are likely to be accompanied by an increase in gastric microcirculation.
腰果酚及其所含的腰果酚酸（AAs）已被证明具有抗氧化、脂氧合酶抑制、抗幽门螺杆菌和抗肿瘤作用。尽管有这些已知的作用，但迄今为止，还没有关于其可能的胃保护作用的报道。本研究旨在验证 AAs 是否对乙醇诱导的胃损伤具有胃保护作用，并研究其潜在的机制。通过胃内给予 0.2mL 乙醇（96%）诱导胃损伤。各组小鼠分别用 AAs（10、30 和 100mg/kg）、米索前列醇（50μg/kg）或载体（2%吐温 80 生理盐水，10mL/kg）预处理，在给予乙醇前 45min 进行预处理。30min 后处死小鼠，取出胃，用面积测定法测量粘膜损伤面积（mm 2 ）。根据抑制胃损伤面积评估胃保护作用。为了研究胃保护机制，分析了其与辣椒素敏感纤维、内源性前列腺素、一氧化氮和三磷酸腺苷敏感钾通道的关系。在胃组织中测量了与乙醇相关的氧化应激标志物 GSH、MDA、过氧化氢酶、SOD 和总硝酸盐/亚硝酸盐水平作为 NO 指标的变化。此外，还分析了 AAs 对 4h 幽门结扎大鼠胃分泌量和总酸度的影响。AAs 对乙醇损伤具有剂量相关的胃保护作用，并进一步防止了乙醇诱导的 GSH、MDA、过氧化氢酶、SOD 和硝酸盐/亚硝酸盐水平的变化。然而，它们不能改变胃分泌或总酸度。观察到 AAs 的胃保护作用在预先用辣椒素、吲哚美辛、L-NAME 或格列本脲预处理的动物中大大降低。这些结果表明，AAs 通过抗氧化机制提供胃保护。其他补充机制包括激活辣椒素敏感胃传入纤维、刺激内源性前列腺素和一氧化氮以及打开 K+（ATP）通道。这些综合作用可能伴随着胃微循环的增加。
