【摘 要】
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Diabetes-induced testicular cell death is predominantly due to oxidative stress.Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is an important transcription factor in controlling the anti-oxidativ
【机 构】
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China-Japan Union Hospital of Jilin University, University of Louisville, Changchun 130000, China
【出 处】
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GTAUF2014 & APSMHA2014第六届长城泌尿男科转化医学论坛暨第七届亚太男性健康与抗衰老研究学会年会
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Diabetes-induced testicular cell death is predominantly due to oxidative stress.Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is an important transcription factor in controlling the anti-oxidative system and is inducible by sulforaphane (SFN).To test whether SFN prevents diabetes-induced testicular cell death, an insulin-defective stage of type 2 diabetes (IDST2DM) was induced in mice.This was accomplished by feeding them a high-fat diet (HFD) for 3 months to induce insulin resistance, and then giving one intraperitoneal injection of streptozotocin to induce hyperglycemia while age-matched control mice were fed a normal diet (ND).IDS-T2DMand ND-fed control mice were then further subdivided into those with or without 4-month SFN treatment.IDS-T2DM induced significant increases in testicular cell death presumably through receptor and mitochondrial pathways, shown by increased ratio of Bax/Bcl2 expression and cleavage of caspase-3 and caspase-8 without significant change of endoplasmic reticulum stress.Diabetes also significantly increased testicular oxidative damage and inflammation.All these diabetic effects were significandy prevented by SFN treatment with up-regulated Nrf2 expression.These results suggest that IDS-T2DM induces testicular cell death presumably through caspase-8 activation and mitochondria-mediated cell death pathways,and also by significantly down-regulating testicular Nrf2 expression and function.SFN up-regulates testicular Nrf2 expression, and its target antioxidant expression, which was associated with significant protection of the testis from IDS-T2DM-induced germ cell death.
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