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本工作研究了在大鼠冷冻加束缚应激性溃疡形成过程中,中枢5-羟色胺(5-HT)通过升高血浆皮质激素水平影响胃粘膜损伤的机制。以血浆和胃粘膜细胞溶酶体内外的组织蛋白酶D活性作为指标,我们观察到,应激180分钟后大鼠血浆中此酶活性明显高于非应激鼠,同时胃粘膜细胞溶酶体内此酶活性下降,说明应激后机体的一些组织受损伤,胃粘膜即为其中之一。如在应激前10分钟向侧脑室注射5-HT(50μg),使应激后血浆的酶活性恢复到非应激水平,但不影响此时的胃粘膜细胞溶酶体内的酶活性。腹腔注射皮质醇(2.4mg/kg)与侧脑室注射5-HT的结果相似。应激后胃粘液粘膜结合量明显下降,如应激前侧脑室注射5-HT或腹腔注射皮质醇均可进一步加重胃粘液减少的程度。这些结果说明,应激时在中枢5-HT作用下引起的皮质激素水平升高,对机体整体有保护性作用,而对胃粘膜细胞不但无有效的特异保护作用,反而减少胃粘液合成,降低胃粘膜的保护功能。
This work studied the mechanism of central 5-hydroxytryptamine (5-HT) affecting gastric mucosal injury by increasing plasma corticosteroid levels in the process of rat freezing and restraint stress ulcer formation. In plasma and gastric mucosal lysosome in vitro and in vivo cathepsin D activity as an indicator, we observed that after 180 minutes of stress in rat plasma was significantly higher than the non-stress rat plasma, and gastric mucosal lysosome in vivo Enzyme activity decreased, indicating that some of the body after stress injury, gastric mucosa is one of them. For example, 5-HT (50 μg) was injected into the lateral ventricle 10 min before the stress to restore the post-stress plasma enzyme activity to the non-stress level but not to affect the enzyme activity in the gastric mucosal lysosome at this time. Intraperitoneal injection of cortisol (2.4 mg / kg) produced similar results to intracerebroventricular injection of 5-HT. Stomach mucus mucosal binding decreased significantly after stress, such as pre-stress lateral ventricle injection of 5-HT or intraperitoneal injection of cortisol can further increase the degree of gastric mucus decreased. These results indicate that the stress caused by the central 5-HT caused by elevated levels of corticosteroids on the body as a whole have a protective effect, but not on gastric mucosal cells not only has no specific protective effect, but reduce gastric mucus synthesis and reduce Gastric mucosal protection.