This study is aiming to investigate the protective effect of glucosamine, risedronate (alone or in combination) on articular cartilage in experimental model of immobilized rat knee. Twenty-five adult male albino rats were divided into five groups (five rats each): control group, immobilized group, glucosamine-treated group, risedronate-treated group, and group treated by a combination of glucosamine and risedronate. The articular cartilage was obtained for histological, immunohistochemical and morphometric studies. The immobilized group showed manifestations of osteoarthritis in the form of significant decrease of articular cartilage thickness with surface erosions, shrunken chondrocytes with pyknotic nuclei and marked manifested fall of chondrocyte number. There was manifested reduction of collagen contents of the articular cartilage using Masson trichrome stain. Safranin O-Fast Green revealed low proteoglycan contents. The collagen type II was also declined. The manikin score was 7.8. Risedronate improved this manifestation slightly more than glucosamine, but combination of booth drugs caused significant improvement of the damaged articular cartilage caused by immobilization. Oral administration of glucosamine and risedronate improved the degenerative changes of rat knee articular cartilage that follow immobilization. This improvement was more remarkable when both drugs were used in combination.
Background: Cisplatin is considered a potent chemotherapeutic drug used in clinical oncology but causes testicular damage as a side effect. Erdosteine is a mucolytic drug possessing an antioxidant capacity. Aim of the Work: The present study was planned to evaluate the possible protective effect of erdosteine against cisplatin-induced testicular toxicity in rats. Material and Methods: Forty adult male albino rats were divided into four groups, ten rats each: control, erdosteine-treated (50 mg/kg body weight/day, orally for 7 days), cisplatin-treated (a single dose of 7mg/ kg intraperitoneally) and erdosteine/cisplatin-treated. Erdosteine was administered 24h before cisplatin injection and was continued until animal sacrifice. Six days after cisplatin administration, all rats were anaesthetized with ether. The scrotum of each animal was incised and the testes were removed and processed to be examined by both the light and scanning electron microscopy. Results: Examination of the testicular specimens of the cisplatin-treated group revealed severe testicular damage with significant reduction in the tubular diameter and germinal epithelium thickness compared to the control group. Shrunken tubules, germ cell loss and apoptotic changes in most of the cells, especially the primary spermatocytes and round spermatids were noticed. The mature spermatids appeared markedly decreased in number and the existing ones showed abnormal forms. Increased interstitial edema and apparent decrease in the Leydig cells were also observed. Erdosteine administration before cisplatin showed amelioration of the testicular architecture. Despite the mild degenerative changes in some spermatogenic cells, cell loss was markedly decreased and most of the tubular lumina were full of mature spermatids. Apparent increase in the Leydig cells and decreased interstitial edema was also noticed. Conclusions: Erdosteine partially protected the rat testes against the cisplatin-induced toxicity most probably via its potent antioxidant and radical scavenging activities.
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