Many reports confirm ulcers as an adverse effect of drugs such as nicorandil and aspirin. The exact responsible mechanisms of ulceration have until now not proved. Mucosal ulcers associated with the onset of ulcer are manifested by an increase in proinflammatory cytokine, excessive prostaglandin, and up-regulation of Endothilin-1 level, which directly impacts the release of leptin. These, released locally within mucosal tissues, have played a role in controlling the extent of local inflammatory responses and processes of mucosal repair.
This study was designed to find out the correlation of plasma leptin and prostaglandin levels as a possible mechanism of oral ulcer formation as an adverse effect of nicorandil. The effect of nicorandil for inducing ulceration was assessed. The plasma leptin and prostaglandin E2 for the tested groups in relation to the studied parameters (gender, and daily body weight change) were estimated in albino rats.
Nicorandil causes mucous membrane damage, inflammation, and ulceration. A significant reduction of plasma leptin level, which was dose-dependent, and a non-significant reduction of serum prostaglandin E2 level. The mechanisms of ulcer induction as an adverse effect of nicorandil can be related to dose-dependant leptin and prostaglandin E2 levels, which affects on repair and healing process.
Keywords: Nicorandil, Leptin, Prostaglandin E2, Ulcer.
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Asthma is chronic inflammatory disease affecting 5% of world population. Characterized by eosinophilic type2 inflammation. FKBP51 immunophilin, important modular protein of glucocorticoid receptor (GR). We aimed to evaluate immunocytochemical localization of GR and FKBP51 in induced sputum cells by using immunocytochemical method and immunofluorescent ant-FKBP51 and anti –GR antibody and estimation of IgE and Type 2 inflammatory cytokine IL-5,IL-13 by ELISA technique.GR in the sputum show non-significant decrease of cytoplasmic distribution of the patient groups and highly significant increase in steroid treated patients and non-significant increase in nuclear distribution in non-steroid, FKBP51 nuclear localization show non-significant i
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Many antiepileptic drugs can be utilized to counteract myoclonic seizure; furthermore, diazepam can be used to oppose such type of seizure; in addition, surrogate therapeutic options such as omega 3 may also be utilized.
In this study, twenty-four (24) mice of both sexes weighing 20-25g were randomly-allocated into 4 groups (6 animals each group) as follows: Group I-
... Show MoreThe incidence of disease and damage will increase, if environmental control and acceptable management practices are not provided during the rearing period. Ascites affect young broilers with rapid growth, and the most critical factor in causing ascites syndrome is the lack of oxygen in body tissues (hypoxia). This research aimed to investigate the effect of olive leaves hydroalcoholic extract and probiotics (LactoFeed) on experimental ascites caused by levothyroxine in male broiler chickens. The present study was an interventional type, and for its implementation, a single-factor design was used in eight groups with 3 replicates. Data were analyzed based on a one-way analysis of variance. Blood parameters of male chick
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Methods: Four groups of eight mice each (n=8) were formed by randomly dividing the animals into the groups, glycerol-induced AKI model group, low-dose CT-treated group (50mg/kg), high-dose CT-treated group (100mg/kg), and control group. The renal functions of mice from all groups were evalua
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... Show MoreInhibition of T cell derived cytokine production could help suppress osteoclast differentiation in inflammatory skeletal disorders. Bisphosphonates are typically prescribed to prevent inflammatory bone loss but are not tolerated by all patients and are associated with an increased risk of osteonecrosis of the jaw. In light of this other anti-resorptives such as phytoestrogens are being considered. However the effect of phytoestrogens on T cell-induced osteoclast formation is unclear. The effect of genistein and coumestrol on activated T cell-induced osteoclastogenesis and cytokine production was therefore examined. Concentrations of genistein and coumestrol (10−7 M) previously shown to directly inhibit osteoclast formation also suppressed
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