Effect of α-lipoic acid on fundic gastric mucosal damage induced by acetyl salicylic acid: a histological study

Introduction α-Lipoic acid (ALA), an endogenous agent, has been shown to combat oxidative stress. Aim of the work The aim of the study was to evaluate the protective effect of ALA on fundic gastric mucosal damage induced by acetyl salicylic acid (ASA). Materials and methods Fifty adult male albino rats were divided into four groups: group I (the control group), group II that received ALA for 2 weeks (subgroup IIa) and for 4 weeks (subgroup IIb), group III that received ASA for 2 weeks (subgroup IIIa) and for 4 weeks (subgroup IIIb), and group IV that received ALA 30 min before ASA for 2 weeks (subgroup IVa) and for 4 weeks (subgroup IVb). At the end of the experiment, specimens from the fundus of the stomach were processed for light and electron microscopic examinations. The mean number of proliferating cell nuclear antigen (PCNA)-positive cells, parietal cells, and the mean thickness of the fundic mucosa were measured and the results were statistically analyzed. Results Examination of sections revealed that ASA for 2 weeks induced widening of the gastric pits and focal mononuclear cellular infiltration. The mucous content of the mucosa was apparently increased and PCNA-positive cells were significantly decreased compared with the control group. ASA for 4 weeks resulted in extensive desquamation, thinning out of the mucosa, and diffuse mononuclear cellular infiltration. The collagen content of the lamina propria showed an apparent increase, whereas the mucous content showed an apparent decrease. The parietal cell count and the PCNA-positive cells were significantly decreased compared with the control group. In ultrathin sections, parietal cells showed cytoplasmic vacuoles, decreased intracellular canaliculi, and mitochondria, whereas the chief cells showed dilated rough endoplasmic reticulum and decreased secretory granules. Concomitant use of ALA showed a histological profile nearly comparable with that of the control group in both subgroups IVa and IVb. Conclusion ALA administration prevented the structural changes of the gastric mucosa induced by ASA.