Abstract
The continuing use of nonsteroidal anti-inflammatory drugs (NSAIDs) usually increases the side effects such as peptic ulcer and acute gastric lesions in the gastrointestinal tract. Cuttlebone (CB), isolated from Sepiella maindroni de Rochebrune, was reported to have antioxidant activities, but its role in the treatment of indomethacin-induced gastric lesions has not yet been confirmed. In this research, we investigate the protective effect of cuttlebone on indomethacin-related ulcers in rats and possible mechanisms. Here, gastric ulcers were induced by oral administration of indomethacin, and then the rats were treated with omeprazole (4 mg/kg) or different doses (750, 1500, and 3000 mg/kg of body weight) of cuttlebone. We evaluated lesion index, inflammation score, and a series of oxidant/antioxidant parameters. The data demonstrated that cuttlebone could protect against gastric ulcers induced by indomethacin in a dose-dependent manner (positive correlation). Also, these effects were associated with attenuating the expression of malonaldehyde (MDA) and increasing the levels of some protective ingredients like epidermal growth factor (EGF), prostaglandin E2 (PGE2), and superoxide dismutase (SOD). Thus, considering its ability to protect indomethacin-induced acute gastric mucosal lesions and the underlying mechanisms, CB might be a potential candidate for treating gastric damage caused by NSAIDs.
Highlights
Nonsteroidal anti-inflammatory drugs (NSAIDs) are proverbially used in rheumatic diseases, cardiovascular diseases, and the control of neoplasia development [1, 2]
COX-1 was reported to be involved in mucus secretion, mucosal blood flow, and the maintenance of the gastric mucosa, while COX-2 serves as an inflammatory factor [3]. us, NSAIDs pose anti-inflammatory effects primarily via COX-2 inhibition, while the adverse effects occur simultaneously followed by COX-1 reduction such as local damage to the gastric mucosa
As one of the NSAIDs, indomethacin is prone to bring about serious side effects such as petechial bleeding, ulcerative lesions, and erosions in the mucosa of stomach despite the function of pain-relieving, anti-inflammatory, and antipyretic properties [4]. e development of the gastric mucosal layer lesions is regulated by the inhibition of prostaglandins and overproduction of free radicals [5]
Summary
Nonsteroidal anti-inflammatory drugs (NSAIDs) are proverbially used in rheumatic diseases, cardiovascular diseases, and the control of neoplasia development [1, 2]. Us, NSAIDs pose anti-inflammatory effects primarily via COX-2 inhibition, while the adverse effects occur simultaneously followed by COX-1 reduction such as local damage to the gastric mucosa. As one of the NSAIDs, indomethacin is prone to bring about serious side effects such as petechial bleeding, ulcerative lesions, and erosions in the mucosa of stomach despite the function of pain-relieving, anti-inflammatory, and antipyretic properties [4]. The inhibition of prostaglandin synthesis by indomethacin causes increased susceptibleness to mucosal lesions and gastroduodenal ulceration, as well as induction of oxidative stress and inflammation [6, 7]. An increase in oxidant levels and a decrease in antioxidant levels exhibit a correlation with the degree of damage to gastric mucosa [8]
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