The Antiapoptotic Effects of Sulphurous Mineral Water and Sodium Hydrosulphide on Diabetic Rat Testes

Sadik, Nermin Abdel Hamid; Elseweidy, Mohamed M.; Shaker, Olfat G.

doi:10.1159/000335803

Cited by 18 publications

(13 citation statements)

References 70 publications

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“…This was accompanied by increased testicular oxidative stress markers, as decreased level of GSH and increased lipid peroxidation content, as well as by increased expression of the apoptotic marker; caspase 3. Previous studies have shown that several compounds possessing antioxidant properties might confer testicular protection against diabetes-induced oxidative stress and/or apoptotic markers, as sulfurous mineral water and sodium hydrosulfide,[17] curcumin,[18] quercetin,[19] ferulic acid,[20] pioglitazone,[21] and melatonin. [22]…”

Section: Discussionmentioning

confidence: 99%

Mechanism of testicular protection of carvedilol in streptozotocin-induced diabetic rats

et al. 2014

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Aims:Male sub-fertility and infertility are major complications of diabetes mellitus. The non-selective β-blocker carvedilol has been reported to have favorable effects on some of the diabetic complications based on its antioxidant and anti-apoptotic effects. This study aims to evaluate the possible testicular protective effect of carvedilol in streptozotocin (STZ)-induced diabetic rat model and its possible mechanisms.Materials and Methods:Diabetes was induced by a single i.p. dose of 65 mg/kg of STZ. In parallel groups of diabetic rats, carvedilol in low and high doses (1 and 10 mg/kg/day orally) were administered for 4 weeks. Oxidative stress markers as reduced glutathione (GSH) and the product of lipid peroxidation; malondialdehyde (MDA) were evaluated in testicular homogenate. The level of expression of the apoptotic marker; caspase 3, was assessed using western blot, followed by densitometric analysis.Results:Induction of diabetes caused distortion of histological normal testicular structure, with decrease (P < 0.05) in GSH and increase (P < 0.05) in MDA, as well as induction of caspase 3 expression. Carvedilol in low or high doses reverted diabetes-induced histological damage, restored antioxidant activity and ameliorated caspase 3 expression.Conclusion:Carvedilol confers testicular protection against diabetes-induced damage through antioxidant and anti-apoptotic mechanisms.

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Section: Discussionmentioning

confidence: 99%

Mechanism of testicular protection of carvedilol in streptozotocin-induced diabetic rats

et al. 2014

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“…Another study pointed to increasing seminiferous tubule wall thickness, germ cell depletion, and Sertoli cell vacuolization in diabetic human testicular biopsies (8) and in diabetic rats (9).…”

Section: Introductionmentioning

confidence: 97%

“…Experimental studies suggested that testicular and erectile dysfunction and spermatogenic disruption in the testis were responsible for the observed low testosterone levels in experimental diabetic animals (9). Control of apoptosis is essential for healthy spermatogenesis in the adult testes (10).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of royal jelly against testicular damage in streptozotocin-induced diabetic rats

Karaca¹,

Demirtaş²,

Karaboğa³

et al. 2015

Turk J Med Sci

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Background/aim: To examine the effects of royal jelly (RJ) on testicular damage in streptozotocin (STZ)-induced diabetic rats. Materials and methods:Eighteen adult Wistar albino rats were used, 6 in each of the 3 treatment groups: Group A: control, Group B: STZ-induced diabetes (untreated), Group C: STZ-induced diabetes plus RJ (400 mg/kg daily for 4 weeks). Diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg). Four weeks after the onset of diabetes, testicular apoptotic cell death was examined using immunohistochemical staining for caspase-3 and Ki67 staining for localization of proliferative cells.Results: Compared with the control, the body and testicular weights of the RJ-treated and untreated diabetic rats were decreased (P < 0.05). The histopathological examination showed a significant increase in degenerative changes in the seminiferous tubules and in spermatogenesis of the STZ-treated rats. In contrast, the RJ treatment group showed near-normal morphology, in addition to an increased intensity of immunohistochemical staining for Ki67-positive cells. Conclusion:Diabetes induced a significant increase in testicular apoptotic cell death (caspase-3-positive cells). Caspase-3-positive cells were significantly decreased in the STZ plus RJ-treated group compared with the untreated STZ-induced diabetic group (P < 0.05).

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“…Spermatogenesis is highly complex and critical process for maintaining male fertility. The continuous self-renewal and differentiation of spermatogonial stem cells (SSC) is the most important step for maintaining sperm production, and this process involves numerous molecules and pathways [10,11].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Fluvastatin on Reproductive Function in Obese Male Rats Induced by High-Fat Diet through Enhanced Signaling of mTOR

Cui

Chen

Zhu

et al. 2017

Cell Physiol Biochem

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Background: Statins can reduce reproductive damage induced by obesity or high-fat diet (HFD), but the specific regulatory mechanisms are largely unknown. Since mTOR/p70s6k sinaling promotes spermatogonia proliferation and spermatogenesis, we hypothesized that this pathway will be involved in the protective effects of statin in HFD-induced reproductive dysfunction. Methods: Male Sprague Dawley rats (3 weeks old) were randomly divided into a control group (standard diet), HFD group, and a fluvastatin group (HFD + fluvastatin at 6mg/kg, once daily by oral gavage). After 8 weeks, body weight was obtain and rats were sacrificed. Weights of the testes, gross morphology, sperm parameters, circulating levels of sex hormones, lipid levels, and tissue mTOR, p-P70s6k were measured. Another set of male rats were treated with rapamycin or vehicle. Flow cytometry was used to detect the spermatogonia marker c-kit and cell cycle. p-P70s6k expression was analyzed by Western blot. Results: HFD not only results in rat obesity but also leads to spermatogenetic damage and fluvastatin was able to partially block the effects of HFD. Fluvastatin also partially reversed the suppression of mTOR and p-p70s6k expresson. Conclusion: Our data suggest that fluvastatin has protective effects on reproductive function in obese male rats most probably through enhanced signaling of mTOR.

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The Antiapoptotic Effects of Sulphurous Mineral Water and Sodium Hydrosulphide on Diabetic Rat Testes

Cited by 18 publications

References 70 publications

Mechanism of testicular protection of carvedilol in streptozotocin-induced diabetic rats

Mechanism of testicular protection of carvedilol in streptozotocin-induced diabetic rats

Protective effects of royal jelly against testicular damage in streptozotocin-induced diabetic rats

Protective Effects of Fluvastatin on Reproductive Function in Obese Male Rats Induced by High-Fat Diet through Enhanced Signaling of mTOR

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