Barbarino F, Togănel E, Brilinschi C, Ciupe I, Pop I, Marinescu I
Third Medical Clinic and Institute of Hygiene and Public Health, Cluj-Napoca, Romania.
Biol Trace Elem Res. 1988 Aug;16(3):253-67. doi: 10.1007/BF02797140.
Experimental studies performed on 227 rats showed that Zn-aspartate and Zn-glycinate administered ip lowered the incidence, number, and severity of the reserpine-induced gastric lesions ensuring significant protection indices. Histochemical methods revealed increased amount of mucosal glycoproteins. The activity of dehydrogenases involved in energy metabolism that modulates acid secretion in the parietal cells was depressed. RNA content in the chief cells, as premises of pepsinogen synthesis, was decreased. ATPase reaction in the periglandular capillaries was uniform and stronger, showing an improvement of gastric mucosal microcirculation. Since these histochemical changes were also noted in healthy rats receiving Zn salts, it might be suggested that they are not the mere expression of an anti-ulcer protective effect of zinc, but rather reflect its mechanism of action, relating to the complex metabolic events induced by the trace element. Our results are in agreement with those previously reported concerning the noxious influence of Zn depletion, the accelerated healing of peptic ulcer patients after Zn treatment, and the protective effect of Zn against ulcerogenesis in several experimental models involving different pathomechanisms.
对227只大鼠进行的实验研究表明,腹腔注射天门冬氨酸锌和甘氨酸锌可降低利血平诱导的胃损伤的发生率、数量和严重程度,确保显著的保护指数。组织化学方法显示黏膜糖蛋白含量增加。参与能量代谢调节壁细胞酸分泌的脱氢酶活性受到抑制。作为胃蛋白酶原合成前提的主细胞中的RNA含量降低。腺周毛细血管中的ATP酶反应均匀且更强,表明胃黏膜微循环得到改善。由于在接受锌盐的健康大鼠中也观察到了这些组织化学变化,可能表明它们并非锌的抗溃疡保护作用的单纯表现,而是反映了其作用机制,与微量元素诱导的复杂代谢事件有关。我们的结果与先前报道的关于锌缺乏的有害影响、锌治疗后消化性溃疡患者愈合加速以及锌在涉及不同发病机制的几种实验模型中对溃疡形成的保护作用的结果一致。