Ameliorating effects of mesenchymal stem cells on testicular injury in a prepubescent rat model of streptozotocin-induced diabetes | ||||
African Journal of Biological Sciences | ||||
Articles in Press, Accepted Manuscript, Available Online from 08 December 2022 | ||||
Document Type: Original Article | ||||
DOI: 10.21608/ajbs.2022.174605.1044 | ||||
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Authors | ||||
Sahar A. Sabry; Samia M. Sakr; Hany N Yousef | ||||
Department of Biological and Geological Sciences, Faculty of Education, Ain Shams University, Cairo, Egypt | ||||
Abstract | ||||
Oxidative stress, inflammation, and apoptosis contribute to testicular dysfunction in diabetes mellitus (DM). Accordingly, the present study aimed to evaluate the potential ameliorative effects of systemic administration of bone marrow mesenchymal stem cells (BM-MSCs) on testicular injury in prepubescent male rats with streptozotocin (STZ)-induced diabetes. A total of 24 four-week-old male albino rats were equally divided into four groups: rats administered normal saline only (control group), STZ-treated rats (diabetes group), STZ-treated rats administered 2×106 BM-MSCs one week after STZ therapy (early MSC treatment group), and rats administered 2×106 BM-MSCs four weeks after STZ injection (late MSC treatment group). At seven days after BM-MSC administration, serum and testicular tissue samples were obtained for biochemical, histological, and ultrastructural analyses. In contrast to the control group, diabetes group showed low levels of testosterone, follicle-stimulating hormone, and luteinizing hormone in sera, and decreased level of glutathione and diminished activities of superoxide dismutase, catalase, and glutathione peroxidase in testicular tissues. In contrast, total oxidant status, thiobarbituric acid reactive substances, tumor necrosis factor-α and interleukin-1β were significantly increased compared to the control group. Histological examination demonstrated hypoplasia and arrest of spermatogenesis at various stages. The cytoplasm of spermatogenic cells was characterized by a high number of defective mitochondria and expanded rough endoplasmic reticula. Early administration of BM-MSCs ameliorated most of the effects of STZ-induced diabetes in testicular tissues. These findings demonstrate that early systemic administration of BM-MSCs to prepubescent rats protects against testicular injury and may restore testicular function in a model of STZ-induced diabetes. | ||||
Keywords | ||||
BM-MSCs; Testis; Oxidative Stress; Proinflammatory Cytokines | ||||
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