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首页> 外文期刊>Ukrainian Biochemical Journal >Lectinocytochemical study of rat stomach mucosa under the conditions of cyclooxygenase-1/-2 blockage and pretreatment witH H-Glu-Asp-Gly-OH
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Lectinocytochemical study of rat stomach mucosa under the conditions of cyclooxygenase-1/-2 blockage and pretreatment witH H-Glu-Asp-Gly-OH

机译：在环氧酶-1 / -2裂缝条件下大鼠胃粘膜的凝集细胞化学研究及H-Glu-ASP-GLY-OH的预处理

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Assessment of glycoconjugate expression on cell membranes using the lectin histochemistry technique may be a feasible approach for evaluating the functional state of the cell. The aim of this study was to evaluate carbohydrate determinants of rat stomach mucosa cell membranes under the conditions of COX-1/-2 blockage with indomethacin and pretreatment with the tripeptide H-Glu-Asp-Gly-OH. Male Wistar rats were divided into 3 groups ( n = 6 per group): 1supst/sup group (control) received vehicle; 2supnd/sup – indomethacin (35 mg/kg); 3suprd/sup – H-Glu-Asp-Gly-OH (10 μg) 30 min before indomethacin. Rats were sacrificed 24 hours later. Gastric mucosa (GM) carbohydrate determinants were studied by lectin-peroxidase technique. The lectins panel included α-fucose- (LABA), syalo- (WGA, SNA), mannose- (Con A, LCA) and galactose-specific (HPA, PNA, SBA) lectins. Intensity of lectin-receptor reaction was scored: 0 – no reaction; 1 – weak; 2 – mild; and 3 – strong reaction. COX-1/2 blockage caused GM lesions, attenuated by H-Glu-Asp-Gly-OH. WGA and SNA showed the highest affinity to GM. Indomethacin decreased SNA-labeling of epitheliocytes and mucocytes and LABA-labeling of chief cells. H-Glu-Asp-Gly-OH reversed the glycosylation changes, caused by COX-1/COX-2 blockage only in regards to labeling of chief cells with LABA, epitheliocytes and mucocytes with LCA, mucocytes with SNA. Predominantly H-Glu-Asp-Gly-OH under COX-1/COX-2 blockage had an effect opposite to indomethacin alone but glycosylation changes under these conditions differed significantly also from the control. COX-1/COX-2 blockage causes alteration of glycosylation processes in rat GM, mainly reduction of NeuNAc(α2-6)DGal and α-Fuc content. H-Glu-Asp-Gly-OH under the conditions of COX-1/COX-2 blockage leads to more profound changes in GM lectin-binding pattern compared to the independent effect of indomethacin and to control.
机译：使用凝集素组织化学技术评估在细胞膜上的糖缀合物表达可以是用于评估细胞功能状态的可行方法。本研究的目的是在Cox-1 / -2裂缝的条件下评估大鼠胃粘膜细胞膜的碳水化合物决定簇，用吲哚美辛和三肽H-glu-ASP-甘氨酸 - 哦预处理。雄性Wistar大鼠分为3组（每组n = 6）：1 st 组（控制）接收车辆; 2 nd - 吲哚美辛（35 mg / kg）; 3 Rd - H-glu-Asp-gly-OH（10μg）在吲哚美辛前30分钟。 24小时后牺牲了大鼠。通过凝集素 - 过氧化物酶技术研究了胃黏膜（GM）碳水化合物决定簇。凝集素面板包括α-岩藻糖（Laba），Syalo-（WGA，SNA），甘露糖 - （CON A，LCA）和半乳糖特异性（HPA，PNA，SBA）凝集素。凝集素受体反应的强度得分：0 - 不反应; 1 - 弱; 2 - 温和;和3 - 强烈反应。 COX-1/2阻塞使GM病变，由H-Glu-ASP-GLY-OH衰减。 WGA和SNA向GM显示了最高的亲和力。吲哚美辛降低了上皮细胞和粘膜标记的SNA标记和粘膜标记的主要细胞。 H-Glu-Asp-Gly-OH逆转糖基化变化，仅由Cox-1 / Cox-2堵塞引起的，仅在用Laba，上皮细胞和粘液用LCA，粘液用SNA标记的标记。在COX-1 / COX-2堵塞下主要是H-Glu-ASP-GLY-OH对单独的吲哚美辛的效果与吲哚美辛相对，但在这些条件下的糖基化变化也显着不同于对照。 COX-1 / COX-2堵塞导致大鼠GM中糖基化方法的改变，主要减少Neunac（α2-6）DGAL和α-FUC含量。 H-Glu-Asp-Gly-OH在Cox-1 / Cox-2堵塞的条件下，与吲哚美辛和控制的独立效果相比，GM凝集素结合模式的更深刻变化。

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