Protective and healing promotion effect of heat shock protein on stress induced gastric ulceration in rats | ||||
| Bulletin of Egyptian Society for Physiological Sciences | ||||
| Article 19, Volume 26, Issue 2, December 2006, Page 305-326 PDF (262.28 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/besps.2006.37584 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
| Nagat Yonan* 1; Samah El-attar2; Laila Elsaid2; Hesham Mahmoud3; Mary Youssef2 | ||||
| 1Professor; Department of physiology; Faculty of Medicine; Cairo University | ||||
| 2Lecturer; Department of Physiology; Faculty of Medicine; Cairo University | ||||
| 3Lecturer; Department of Pharmacology; Faculty of Medicine; Cairo University | ||||
| Abstract | ||||
| Background: Heat shock proteins play an important role in the maintenance of normal cell integrity and also serve to protect cells from the cytotoxic effects of aggregated proteins produced by various stresses. Water immersion and restraint stress (WRS) induces gastric ulceration. Treatment with non steroidal antiinflammatory drugs or blocking nitric oxide “NO” synthesis by L-NAME, a NO synthase inhibitor, aggravates gastric ulceration. On the other hand heat preconditioning or treatment with NO donor, L-arginine, act as cyto-protective factors protecting the gastric mucosa and enhance gastric mucosal healing. However, whether the pathogenic effects of aspirin and L-NAME, and the cyto-protective effect of NO and heat preconditioning are related to their effect on expression of heat shock protein-70 (HSP70) in gastric mucosa or not is still undetermined. Aim of work: The present study was established to investigate the potential participation of HSP70 in the protection against acute gastric mucosal damage and its role in recovery, also the effect of acetyl salicylic acid, NO and heat preconditioning on its release and effect. Methods: 128 male albino rats were divided into 6 groups, 24 rats each (except group-I comprised of 8 rats); Group-I: control non stressed group, rats received oral vehicle (saline) 1ml/rat, the rats in the stressed groups II-VI were pretreated 30 min. before the start of WRS by different factors. Group-II: rats received oral vehicle (saline 1ml/rat). Group-III: rats are heat preconditioned at 42°C for 30 min. Group- IV: rats received acetyl salicylic acid (ASA, aspirin) orally (40mg/kg). Group-V: rats received oral L-arginine (250 mg/kg). Group-VI: rats received oral L-NAME (10 mg/kg). All rats were exposed to WRS (except group-I) for 3.5 hours, then all rats were sacrificed, including group-I, then number of gastric ulcers, gastric malondialdehyde (MDA) content “an indicator for lipid peroxidation in gastric mucosa”, and expression of inducible NO synthase (iNOS) and HSP70 in the stomach were determined at 0, 6, 24 hours after the end of WRS. Results: WRS caused typical bleeding erosions and that were aggravated by ASA and L-NAME pretreatment and this was accompanied by a significant rise in MDA, and a significant decrease in the expression of HSP70. Pretreatment by heat preconditioning or L-arginine resulted in a significant reduction in the number gastric ulceration and promotion of healing with a significant decrease in gastric level of MDA and significant increase in the expression of iNOS and HSP70 in the gastric mucosa. Conclusion: HSP70 has a healing promotion effect on induced gastric ulcer in WRS rats and the increase in its expression resulted in a protective effect against the development of the ulcer. It appears that HSP 70 expression alteration is one of the mechanisms by which heat preconditioning, aspirin, L-arginine, and L-NAME induced their effects on gastric mucosa. | ||||
| Keywords | ||||
| Stress ulcers; L-NAME; L-arginine; Acetyl salicylic acid; Heat shock proteins (HSP) | ||||
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