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[抗酸包衣剂对大鼠的胃保护作用。内源性前列腺素、辣椒素敏感传入神经元和一氧化氮的作用]

[Gastroprotective effect of an antacid coating agent in rats. Role of endogenous prostaglandins, capsaicin-sensitive afferents neurons and nitric oxide].

作者信息

Ramaholimihaso F, Duchateau A, Scheck F, Thiefin G

机构信息

Laboratoire de Morphologie Cellulaire Digestive, UFR Médecine de Reims.

出版信息

Gastroenterol Clin Biol. 1997;21(5):370-6.

PMID:9208012
Abstract

UNLABELLED

The aims of this study were: a) to demonstrate the gastroprotective effect of the antacid and mucosal coating agent Gastralgine (aluminium hydroxide and glycinate, magnesium trisilicate and simeticone) against ethanol- and indomethacin-induced gastric injury in the rat; b) to investigate whether gastroprotection elicited by this agent involves stimulation of capsaicin sensitive afferent neurons and activation of the nitric oxide system.

METHODS

Rats received intragastrically 2 mL of the antacid or distilled water followed 1 hr later by 2 mL of 100% ethanol ig or 30 mg of indomethacin sc. The surface of ethanol-induced lesions and the length of indomethacin-induced lesions were measured. The role of afferent neurons and endogenous nitric oxide in the prevention of ethanol-induced gastric damage was determined using respectively capsaicin and the inhibitor of nitric oxide biosynthesis, NG-nitro-L-arginine.

RESULTS

The antacid and mucosal coating agent significantly reduced the area of macroscopic lesions induced by ethanol and the length of lesions induced by indomethacin. Both functional ablation of afferent nerves and inhibition of nitric oxide synthesis significantly increased ethanol-induced gastric injury but failed to reverse the gastroprotective effect of the antacid against 100% ethanol.

CONCLUSIONS

The antacid and mucosal coating agent Gastralgine has a gastroprotective effect against ethanol- and indomethacin-induced injury in the rat. This property does not involve stimulation of capsaicin sensitive afferent neurons or synthesis of endogenous nitric oxide.

摘要

未标注

本研究的目的是:a)证明抗酸和黏膜保护剂胃喜(氢氧化铝甘氨酸盐、三硅酸镁和西甲硅油)对大鼠乙醇和吲哚美辛诱导的胃损伤具有胃保护作用;b)研究该药物引起的胃保护作用是否涉及辣椒素敏感传入神经元的刺激和一氧化氮系统的激活。

方法

大鼠经胃内给予2 mL抗酸剂或蒸馏水,1小时后经胃内给予2 mL 100%乙醇或经皮下给予30 mg吲哚美辛。测量乙醇诱导损伤的面积和吲哚美辛诱导损伤的长度。分别使用辣椒素和一氧化氮生物合成抑制剂NG-硝基-L-精氨酸来确定传入神经元和内源性一氧化氮在预防乙醇诱导的胃损伤中的作用。

结果

抗酸和黏膜保护剂显著减少了乙醇诱导的宏观损伤面积和吲哚美辛诱导的损伤长度。传入神经的功能性消融和一氧化氮合成的抑制均显著增加了乙醇诱导的胃损伤,但未能逆转抗酸剂对100%乙醇的胃保护作用。

结论

抗酸和黏膜保护剂胃喜对大鼠乙醇和吲哚美辛诱导的损伤具有胃保护作用。该特性不涉及辣椒素敏感传入神经元的刺激或内源性一氧化氮的合成。

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