al-Swayeh O A, Ali A T
Department of Medical Pharmacology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Hepatogastroenterology. 1998 Jan-Feb;45(19):297-302.
BACKGROUND/AIMS: Accumulating evidence indicates that capsaicin-sensitive afferent neurons play a pivotal role in acute gastroprotection by liberating vasodilator substances. The mechanism of gastric protection by honey and sucralfate has been shown to be mediated through the vasodilator nitric oxide and cytoprotective sulphydryl-sensitive pathways in the stomach. The aim of the present study was to investigate the role of capsaicin-sensitive afferent neurons in the protective mechanism of honey and sucralfate against ethanol-induced gastric lesions.
Ablation of capsaicin-sensitive afferent neurons was carried out by treating rats with neurotoxic doses of capsaicin (50 + 50 mg/kg subcutaneously over 2 consecutive days). The control groups received equal volumes of the vehicle (10% ethanol + 10% Tween 80 + 80% normal saline). The non-protein sulphydryl level was determined spectrophotometrically.
Afferent sensory nerve ablation significantly aggravated ethanol-induced gastric lesions and caused a greater depletion of non-protein sulphydryl levels. Pretreatment with honey (0.078-0.625 g/kg, orally) or sucralfate (0.062-0.250 g/kg, orally) 30 min before administration of the ethanol prevented ethanol-induced gastric lesions and the depletion of non-protein sulphydryls in vehicle-treated rats. However, honey failed to afford protection or reverse non-protein sulphydryl depletion, while sucralfate was effective in the capsaicin-treated animals. The protective effect of sucralfate was lost in both groups following pretreatment with indomethacin (10 mg/kg, subcutaneously), while honey-induced protection was unaffected.
These results suggest that the gastric protection by honey is solely dependent on the presence of intact afferent sensory neurons, whereas sucralfate-induced gastroprotection is mediated through the afferent sensory neuron and prostaglandin systems. It seems that the non-protein sulphydryl level is affected by the ablation of sensory neurons and plays an important regulatory role in gastric protection.
背景/目的：越来越多的证据表明，对辣椒素敏感的传入神经元通过释放血管舒张物质在急性胃保护中起关键作用。蜂蜜和硫糖铝的胃保护机制已被证明是通过胃中血管舒张性一氧化氮和细胞保护硫氢基敏感途径介导的。本研究的目的是探讨对辣椒素敏感的传入神经元在蜂蜜和硫糖铝对乙醇诱导的胃损伤的保护机制中的作用。
通过用神经毒性剂量的辣椒素（连续2天皮下注射50 + 50 mg/kg）处理大鼠来消除对辣椒素敏感的传入神经元。对照组接受等量的赋形剂（10%乙醇 + 10%吐温80 + 80%生理盐水）。用分光光度法测定非蛋白硫氢基水平。
传入感觉神经切除显著加重了乙醇诱导的胃损伤，并导致非蛋白硫氢基水平的更大消耗。在给予乙醇前30分钟口服蜂蜜（0.078 - 0.625 g/kg）或硫糖铝（0.062 - 0.250 g/kg）可预防乙醇诱导的胃损伤以及赋形剂处理大鼠中非蛋白硫氢基的消耗。然而，蜂蜜未能提供保护或逆转非蛋白硫氢基的消耗，而硫糖铝在辣椒素处理的动物中是有效的。在皮下注射吲哚美辛（10 mg/kg）预处理后，两组中硫糖铝的保护作用均丧失，而蜂蜜诱导的保护作用未受影响。
这些结果表明，蜂蜜的胃保护作用完全依赖于完整的传入感觉神经元的存在，而硫糖铝诱导的胃保护作用是通过传入感觉神经元和前列腺素系统介导的。似乎非蛋白硫氢基水平受感觉神经元切除的影响，并在胃保护中起重要的调节作用。
