ArticleJournal of gastroenterology2007
Effects of leptin on stress-induced changes of caspases in rat gastric mucosa.
Article in Journal of gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 4 citations in OpenAlex.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn this study, we investigated the effect of leptin on caspase-3, caspase-8, and caspase-9 immunoreactivity and lipid peroxidation in the stomachs of rats exposed to cold-restraint stress.
methodsThirty-two male Wistar Albino rats were used. Rats pretreated with leptin (10 microg/kg per day for 7 days) were restrained in a wire cage for 4 h at 4 degrees C. Spectrophotometric techniques were used for detection of malondialdehyde (MDA) and glutathione (GSH) levels, and immunoreactivity of caspases was investigated by immunohistochemistry.
resultsWhile the stomach MDA level of the cold-restraint stress group was increased significantly, the level of GSH was decreased when compared with the control group. Caspase-9 and caspase-3 immunoreactivities of the stress group were not changed, while caspase-8 immunoreactivity was decreased. Leptin administration prevented the increase in the MDA level and the decrease in the GSH content of the gastric mucosa in animals subjected to stress. Leptin administration produced no significant change in caspase-8 immunoreactivity but caused a decrease in caspase-3 immunoreactivity.
conclusionsCold-restraint stress decreases the antioxidant capacity of stomach tissue while activating oxidants, and induces apoptosis by an increase in caspase immunoreactivity. The presence of leptin reverses these mechanisms and suppresses the apoptosis.
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