Hill Tracy L, Blikslager Anthony T
Department of Clinical Science, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27607, USA.
Am J Vet Res. 2012 May;73(5):659-63. doi: 10.2460/ajvr.73.5.659.
To examine whether a zinc L-carnosine compound used for treatment of suspected gastric ulcers in dogs ameliorates acid-induced injury in canine gastric mucosa.
Gastric mucosa from 6 healthy dogs.
Mucosa from the gastric antrum was harvested from 6 unadoptable shelter dogs immediately after euthanasia and mounted on Ussing chambers. The tissues were equilibrated for 30 minutes in neutral Ringer's solution prior to incubation with acidic Ringer's solution (HCl plus Ringer's solution [final pH, 1.5 to 2.5]), acidic Ringer's solution plus zinc L-carnosine compound, or zinc L-carnosine compound alone. Tissues were maintained for 180 minutes in Ussing chambers, during which permeability was assessed by measurement of transepithelial electrical resistance. After the 180-minute treatment period, tissues were removed from Ussing chambers and labeled with immunofluorescent anti-active caspase-3 antibody as an indicator of apoptosis.
Permeability of the gastric mucosa was significantly increased in a time-dependent manner by addition of HCl, whereas control tissues maintained viability for the study period. Change in permeability was detected within the first 15 minutes after acid application and progressed over the subsequent 150 minutes. The zinc L-carnosine compound had no significant effect on this increase in permeability. Apoptosis was evident in acid-treated tissues but not in control tissues. The zinc L-carnosine compound did not protect against development of apoptosis.
Addition of HCl caused a dose-dependent increase in gastric permeability over time and apparent induction of apoptosis as determined on the basis of immunofluorescence. However, there was no significant protective effect of a zinc L-carnosine compound. Nonetheless, results suggested the utility of this method for further studies of canine gastric injury.
研究一种用于治疗犬类疑似胃溃疡的锌 - 肌肽化合物是否能改善酸诱导的犬胃黏膜损伤。
6只健康犬的胃黏膜。
在6只安乐死的流浪犬安乐死后立即采集胃窦黏膜，并安装在尤斯灌流小室中。在与酸性林格氏液（盐酸加林格氏液[最终pH值为1.5至2.5]）、酸性林格氏液加锌 - 肌肽化合物或单独的锌 - 肌肽化合物孵育之前，将组织在中性林格氏液中平衡30分钟。组织在尤斯灌流小室中维持180分钟，在此期间通过测量跨上皮电阻评估通透性。在180分钟的治疗期后，将组织从尤斯灌流小室中取出，并用免疫荧光抗活性半胱天冬酶 - 3抗体标记作为细胞凋亡的指标。
添加盐酸后，胃黏膜的通透性以时间依赖性方式显著增加，而对照组织在研究期间保持活力。在施加酸后的前15分钟内检测到通透性变化，并在随后的150分钟内持续变化。锌 - 肌肽化合物对这种通透性增加没有显著影响。细胞凋亡在酸处理的组织中明显，但在对照组织中不明显。锌 - 肌肽化合物不能预防细胞凋亡的发生。
添加盐酸导致胃通透性随时间呈剂量依赖性增加，并根据免疫荧光确定明显诱导细胞凋亡。然而，锌 - 肌肽化合物没有显著的保护作用。尽管如此，结果表明该方法在犬胃损伤的进一步研究中具有实用性。
