Protective and healing promotion effect of heat shock protein on stress induced gastric ulceration in rats

Document Type : Original Article

Authors

1 Professor; Department of physiology; Faculty of Medicine; Cairo University

2 Lecturer; Department of Physiology; Faculty of Medicine; Cairo University

3 Lecturer; 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

Bulletin of Egyptian Society for Physiological Sciences
Volume 26, Issue 2
December 2006
Pages 305-326

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