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The protective effect of 5-HT3 receptor antagonist in thyrotropin releasing hormone-induced gastric lesions
1Marmara University, Medical Faculty, Department of Pharmacology, Haydarpasa-Istanbul, Turkey.
Abstract:
The present study examined 1) oxidative stress and gastric lesions induced by thyrotropin releasing hormone (TRH) 2) The effect of a 5-hydroxytryptamine3 (5-HT3) receptor antagonist, ICS 205930 on protective effect of calcitonin on gastric lesions produced by TRH. Calcitonin (5 micrograms/10 microliter) was injected i.c.v. 10 min before TRH (10 micrograms/10 microliter, i.c.v.) injection or ICS 0.5 mg/kg, (i.p.) was given 60 min prior to calcitonin or TRH to rats. Ulcer index, lipid peroxidation (LP) and glutathione (GSH) levels were quantified 3 h after TRH injection in the stomach, liver and brain. TRH caused mucosal lesions (UI: 10.0 +/- 2.0 mm) without changing gastric GSH and LP. JCS did not alter the protective effect of calcitonin against TRH-induced lesions but attenuated. TRH-induced lesion formation. The oxidative effects of calcitonin or ICS were similar to TRH but both drugs attenuated gastric lesion formation. Hence, oxidative changes in tissues studied are not directly involved in TRH-induced lesions.
Insights
Thyrotropin-releasing hormone (TRH) causes gastric lesions, but not through oxidative stress. Calcitonin and a 5-HT3 antagonist (ICS 205930) protect against these lesions, suggesting non-oxidative mechanisms are involved.
Area of Science:
- Gastroenterology
- Neuroendocrinology
- Pharmacology
Background:
- Thyrotropin-releasing hormone (TRH) is implicated in gastric mucosal injury.
- Oxidative stress markers are often associated with gastrointestinal lesions.
- Calcitonin and 5-HT3 receptor antagonists are potential therapeutic agents for gastric protection.
Purpose of the Study:
- To investigate the role of oxidative stress in TRH-induced gastric lesions.
- To evaluate the protective effects of calcitonin against TRH-induced gastric damage.
- To determine the influence of the 5-HT3 receptor antagonist ICS 205930 on calcitonin's protective action and TRH-induced lesions.
Main Methods:
- Rats were administered calcitonin and/or TRH intracerebroventricularly (i.c.v.).
- The 5-HT3 antagonist ICS 205930 was administered intraperitoneally (i.p.) before other treatments.
- Gastric ulcer index, lipid peroxidation (LP), and glutathione (GSH) levels were measured in stomach, liver, and brain tissues.
Main Results:
- TRH induced significant gastric mucosal lesions (Ulcer Index: 10.0 ± 2.0 mm).
- TRH did not alter gastric glutathione or lipid peroxidation levels.
- ICS 205930 did not affect calcitonin's protective effect but attenuated TRH-induced lesion formation; both calcitonin and ICS showed oxidative effects similar to TRH but reduced gastric lesions.
Conclusions:
- Oxidative changes in the studied tissues are not directly implicated in TRH-induced gastric lesion formation.
- Calcitonin and ICS 205930 demonstrate protective effects against TRH-induced gastric lesions through mechanisms independent of direct modulation of gastric oxidative stress.
- Further research is warranted to elucidate the precise non-oxidative pathways involved in TRH-induced gastric injury and the protective actions of calcitonin and 5-HT3 antagonists.