Aims: Asthma is an inflammatory lung disease characterized by bronchoconstriction and hyper responsiveness. Immuno stimulatory effects of melatonin have been reported. In this study, we investigated the impact of melatonin administration on allergic airway inflammation in a rat model. Methods: Forty five adult Wistar albino rats were equally divided into three groups: group I served as control; group II: rats sensitized to ovalbumin and challenged intranasally with ovalbumin to induce an allergic inflammatory response and group III, rats were sensitized and treated with intraperitoneally melatonin. The serum levels of IgE, IgG1 and ova-specific IgG were measured by ELISA. In the bronchoalveolar lavage fluid (BALF), the levels of IL-4, IL-5, IL-13, 1L-10 were measured. IL-10 expression was measured by real time polymerase chain reaction. Histopathological examination of the lung tissues using H&E stain were done. Results: Melatonin administration inhibited allergen-induced lung eosinophilic infiltration and improved the pathological lesions of the lungs. It significantly decreased total serum IgE, IgG1 and OVA-specific IgG1 along with BALF levels of IL-4, IL-5, IL-13. Melatonin increased BALF levels of IL-10 and its mRNA expression. Conclusion: Melatonin administration exhibited a significant reduction in all the markers of allergic inflammation. The data suggests that inhibition of T-cell response and up regulation of IL-10 may be responsible for immunomodulatory effect of melatonin in the rat model of allergic airway inflammation.

Aims: Asthma is an inflammatory lung disease characterized by bronchoconstriction and hyper responsiveness. Immuno stimulatory effects of melatonin have been reported. In this study, we investigated the impact of melatonin administration on allergic airway inflammation in a rat model. Methods: Forty five adult Wistar albino rats were equally divided into three groups: group I served as control; group II: rats sensitized to ovalbumin and challenged intranasally with ovalbumin to induce an allergic inflammatory response and group III, rats were sensitized and treated with intraperitoneally melatonin. The serum levels of IgE, IgG1 and ova-specific IgG were measured by ELISA. In the bronchoalveolar lavage fluid (BALF), the levels of IL-4, IL-5, IL-13, 1L-10 were measured. IL-10 expression was measured by real time polymerase chain reaction. Histopathological examination of the lung tissues using H&E stain were done. Results: Melatonin administration inhibited allergen-induced lung eosinophilic infiltration and improved the pathological lesions of the lungs. It significantly decreased total serum IgE, IgG1 and OVA-specific IgG1 along with BALF levels of IL-4, IL-5, IL-13. Melatonin increased BALF levels of IL-10 and its mRNA expression. Conclusion: Melatonin administration exhibited a significant reduction in all the markers of allergic inflammation. The data suggests that inhibition of T-cell response and up regulation of IL-10 may be responsible for immunomodulatory effect of melatonin in the rat model of allergic airway inflammation.

This study was conducted to investigate the possible protective role of thymoquinone (TQ) and l-cysteine on the reproductive toxicity of male rats induced by cadmium chloride (CdCl2). Forty rats were divided into four even groups. The first group served as untreated control. The second, third and fourth groups received CdCl2, CdCl2 and TQ, and CdCl2 and l-cysteine, respectively for 56 days. Cd exposure caused spermatological damage (decrease sperm count and motility and increased the rates of sperm abnormalities), decrease serum testosterone level and increased oxidative stress. Histological alterations were also observed in the form of vascular and cellular changes in CdCl2 treated rats. The vascular changes were congestion of the blood vessels with interstitial edema in the testes, epididymis, seminal vesicle and prostate. The cellular changes were in the form of degenerative changes with presence of multinucleated giant cells in the lumen of seminiferous tubules, vacuolation and sloughing of the lining epithelium of the epididymis, seminal vesiculitis and prostatitis. Co-administration of TQ and l-cysteine with CdCl2 increased glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and testosterone and reduced lipid peroxidation (LPO) activity. In conclusion, our results showed that TQ and l-cysteine can ameliorate the deleterious effects of CdCl2 probably by activating testicular endocrine and antioxidant systems.

This study was conducted to investigate the possible protective role of thymoquinone (TQ) and l-cysteine on the reproductive toxicity of male rats induced by cadmium chloride (CdCl2). Forty rats were divided into four even groups. The first group served as untreated control. The second, third and fourth groups received CdCl2, CdCl2 and TQ, and CdCl2 and l-cysteine, respectively for 56 days. Cd exposure caused spermatological damage (decrease sperm count and motility and increased the rates of sperm abnormalities), decrease serum testosterone level and increased oxidative stress. Histological alterations were also observed in the form of vascular and cellular changes in CdCl2 treated rats. The vascular changes were congestion of the blood vessels with interstitial edema in the testes, epididymis, seminal vesicle and prostate. The cellular changes were in the form of degenerative changes with presence of multinucleated giant cells in the lumen of seminiferous tubules, vacuolation and sloughing of the lining epithelium of the epididymis, seminal vesiculitis and prostatitis. Co-administration of TQ and l-cysteine with CdCl2 increased glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and testosterone and reduced lipid peroxidation (LPO) activity. In conclusion, our results showed that TQ and l-cysteine can ameliorate the deleterious effects of CdCl2 probably by activating testicular endocrine and antioxidant systems.

The present study aims to investigate the protective effects of thymoquinone, the major active ingredient of Nigella sativa seeds, against lead-induced brain damage in Sprague-Dawley rats. In which, 40 rats were divided into four groups (10 rats each). The first group served as control. The second, third and fourth groups received lead acetate, lead acetate and thymoquinone, and thymoquinone only, respectively, for one month. Lead acetate was given in drinking water at a concentration of 0.5 g/l (500 ppm). Thymoquinone was given daily at a dose of 20 mg/kg b.w. in corn oil by gastric tube. Control and thymoquinone-treated rats showed normal brain histology. Treatment of rats with lead acetate was shown to produce degeneration of endothelial lining of brain blood vessels with peri-vascular cuffing of mononuclear cells consistent to lymphocytes, congestion of choroid plexus blood vessels, ischemic brain infarction, chromatolysis and neuronal degeneration, microglial reaction and neuronophagia, degeneration of hippocampal and cerebellar neurons, and axonal demyelination. On the other hand, co-administration of thymoquinone with lead acetate markedly decreased the incidence of lead acetate-induced pathological lesions. Thus the current study shed some light on the beneficial effects of thymoquinone against neurotoxic effects of lead in rats.The present study aims to investigate the protective effects of thymoquinone, the major active ingredient of Nigella sativa seeds, against lead-induced brain damage in Sprague-Dawley rats. In which, 40 rats were divided into four groups (10 rats each). The first group served as control. The second, third and fourth groups received lead acetate, lead acetate and thymoquinone, and thymoquinone only, respectively, for one month. Lead acetate was given in drinking water at a concentration of 0.5 g/l (500 ppm). Thymoquinone was given daily at a dose of 20 mg/kg b.w. in corn oil by gastric tube. Control and thymoquinone-treated rats showed normal brain histology. Treatment of rats with lead acetate was shown to produce degeneration of endothelial lining of brain blood vessels with peri-vascular cuffing of mononuclear cells consistent to lymphocytes, congestion of choroid plexus blood vessels, ischemic brain infarction, chromatolysis and neuronal degeneration, microglial reaction and neuronophagia, degeneration of hippocampal and cerebellar neurons, and axonal demyelination. On the other hand, co-administration of thymoquinone with lead acetate markedly decreased the incidence of lead acetate-induced pathological lesions. Thus the current study shed some light on the beneficial effects of thymoquinone against neurotoxic effects of lead in rats.

The present study aims to investigate the protective effects of thymoquinone, the major active ingredient of Nigella sativa seeds, against lead-induced brain damage in Sprague-Dawley rats. In which, 40 rats were divided into four groups (10 rats each). The first group served as control. The second, third and fourth groups received lead acetate, lead acetate and thymoquinone, and thymoquinone only, respectively, for one month. Lead acetate was given in drinking water at a concentration of 0.5 g/l (500 ppm). Thymoquinone was given daily at a dose of 20 mg/kg b.w. in corn oil by gastric tube. Control and thymoquinone-treated rats showed normal brain histology. Treatment of rats with lead acetate was shown to produce degeneration of endothelial lining of brain blood vessels with peri-vascular cuffing of mononuclear cells consistent to lymphocytes, congestion of choroid plexus blood vessels, ischemic brain infarction, chromatolysis and neuronal degeneration, microglial reaction and neuronophagia, degeneration of hippocampal and cerebellar neurons, and axonal demyelination. On the other hand, co-administration of thymoquinone with lead acetate markedly decreased the incidence of lead acetate-induced pathological lesions. Thus the current study shed some light on the beneficial effects of thymoquinone against neurotoxic effects of lead in rats.The present study aims to investigate the protective effects of thymoquinone, the major active ingredient of Nigella sativa seeds, against lead-induced brain damage in Sprague-Dawley rats. In which, 40 rats were divided into four groups (10 rats each). The first group served as control. The second, third and fourth groups received lead acetate, lead acetate and thymoquinone, and thymoquinone only, respectively, for one month. Lead acetate was given in drinking water at a concentration of 0.5 g/l (500 ppm). Thymoquinone was given daily at a dose of 20 mg/kg b.w. in corn oil by gastric tube. Control and thymoquinone-treated rats showed normal brain histology. Treatment of rats with lead acetate was shown to produce degeneration of endothelial lining of brain blood vessels with peri-vascular cuffing of mononuclear cells consistent to lymphocytes, congestion of choroid plexus blood vessels, ischemic brain infarction, chromatolysis and neuronal degeneration, microglial reaction and neuronophagia, degeneration of hippocampal and cerebellar neurons, and axonal demyelination. On the other hand, co-administration of thymoquinone with lead acetate markedly decreased the incidence of lead acetate-induced pathological lesions. Thus the current study shed some light on the beneficial effects of thymoquinone against neurotoxic effects of lead in rats.

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