Streptozotocin-induced diabetes increases the interaction of Bad/Bcl-XL and decreases the binding of pBad/14–3–3 in rat testis

Koh, Phil-Ok

doi:10.1016/j.lfs.2007.08.017

Cited by 35 publications

(22 citation statements)

References 27 publications

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“…Our TUNEL data clearly indicate that the increase in the number of TUNEL-positive cells in the diabetic group led to damage in the spermatocytes as compared to the control. It has been reported that the increase in the apoptotic cell death in the testis is mediated through the regulation of Bcl-2 family proteins and by the activation of JNK and Bax pathways in STZ-induced diabetic rat (Koh 2007b). Furthermore, the expression of NFκB and COX-2 levels was found to be increased in the diabetic testes as compared to the control, which was ameliorated by the intervention with enalapril.…”

Section: Discussionmentioning

confidence: 88%

Enalapril reduces germ cell toxicity in streptozotocin-induced diabetic rat: investigation on possible mechanisms

Kushwaha

Jena

2011

Naunyn-Schmiedeberg's Arch Pharmacol

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Diabetes mellitus, a state of persistent hyperglycemia, is a major cause of micro- and macrovascular diseases. It affects nearly every system in the body including the reproductive system. Abnormalities in spermatogenesis and sexual function have been documented in animal models for both types of diabetes. The purpose of the present study is to determine the possible protective effects of enalapril against the germ cell toxicity in diabetic rat. Sprague-Dawley rats were divided into four groups: (1) control, (2) control + enalapril, (3) diabetic, and (4) diabetic + enalapril. Enalapril was administered per orally for 4 and 8 weeks continuously. After the treatment, animals were sacrificed and blood glucose level, sperm count, sperm DNA damage, apoptotic cell death, immunohistochemistry of 8-oxo- 7,8-dihydro- 2'-deoxyguanosine, and the cellular toxicity were performed. Furthermore, western blotting was performed to evaluate the expression of NFκB and COX-2 in testes. The results of the present study indicate that intervention of enalapril ameliorates the sperm DNA damage, reduces the oxidative stress, and down-regulates the expression of NFκB and COX-2 expression in streptozotocin-induced diabetic rat.

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Section: Discussionmentioning

confidence: 88%

Enalapril reduces germ cell toxicity in streptozotocin-induced diabetic rat: investigation on possible mechanisms

Kushwaha

Jena

2011

Naunyn-Schmiedeberg's Arch Pharmacol

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“…by diabetes [28][29]. Plasma levels of ghrelin are affected by nutritional status implicating a role in regulating energy balance.…”

Section: Discussionmentioning

confidence: 99%

The effects of streptozotocin-induced diabetes on ghrelin expression in rat testis: biochemical and immunohistochemical study

Sönmez

Karabulut

Kilic

et al. 2015

Folia Histochem Cytobiol.

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Introduction. Ghrelin is a hormone which has effects on the secretion of growth hormone, gastrointestinal system, cardiovascular system, cell proliferation and reproductive system. The present study we focused on the relation between ghrelin and GHS-R1a gene expression and the regulation of their expression in the testes of diabetic rats. Material and methods. 40 male Wistar albino rats were divided into four groups: control, and sampled 4, 8 and 12 weeks after induction of diabetes by streptozotocin (STZ) intraperitoneal injection (40 mg/kg). The rats were decapitated under ketamine anesthesia and their testes were removed. Blood was obtained from heart and serum follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were measured by ELISA. Tissue ghrelin and GHS-R mRNA levels were determined by qRT-PCR, while ghrelin protein expression was studied by immunohistochemistry. Histopathological damage scores were also assessed. Results. Eight weeks after diabetes induction serum FSH level was increased, whereas LH and testosterone concentrations decreased. The ghrelin and GHS-R1a gene expression and ghrelin immunohistochemistry score first tended to increase after first four weeks of diabetes, and then tended to decrease. Ghrelin-immunopositive cells were detected in Leydig cells in all groups of rats, however, not in the germinal epithelium. Congestion of vessels and hemorrhage, formation of the vacuoles in spermatogonia and spermatocytes, desquamation of spermatids in the lumen and disorganization of seminiferous tubule germinal epithelium were observed in testis of all the diabetic rats. In addition, mean testicular biopsy score and mean seminiferous tubule diameter were getting lower in diabetic animals. Conclusion. Our results suggest that diabetes affects ghrelin expression in rat testis.

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“…The most frequent effects of DM on the male reproductive system include decreased levels of testosterone, lower testicular weight, abnormal spermatogenesis, alterations in sperm count and motility, and histopathological changes in testis tissue components [2][3][4][5] . Abnormalities in spermatogenesis due to increased apoptosis have been demonstrated in certain studies 2,3,[6][7][8][9][10] . Testicular apoptosis may be the major component of the infertility.…”

Section: Introductionmentioning

confidence: 99%

MAPK immunoreactivity in streptozotocin-induced diabetic rat testis

2014

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PURPOSE:To evaluate the alterations of two mitogen-activated protein kinases (MAPK)s, extracellular signal regulated kinase (ERK) and c-Jun NH2 terminal kinase (JNK), in the testes of male rats with experimental diabetes. METHODS:Twenty males Sprague-Dawley rats were randomly divided into a control group (n=8) and a diabetes group (administration of 40 mg/kg/day streptozotocin (STZ) for five sequential days, n=12). After six weeks, testicular biopsy samples were obtained for light microscopy and immunohistochemical methods. RESULTS:The PCNA (proliferating cell nuclear antigen) index was significantly decreased in the diabetes group (p=0.004) when compared to the control group. Both total (t)-ERK and phosphor (p)-ERK immunoreactivities were significantly decreased in the diabetes group (p=0.004, p<0.001, respectively). The t-JNK immunoreactivity was unchanged in both groups (p=0.125), while p-JNK immunoreactivity was significantly increased in the diabetic group (p=0.002). CONCLUSIONS:The decrease of androgen levels in the course of diabetes may contribute to the decrease of the immunoreactivities of t-ERK and p-ERK. JNK may be activated due to the changes in various cytokines and chemochines that participate in the oxidative stress process of diabetes. Therefore, testicular apoptosis may occur and lead to infertility associated with diabetes.

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Streptozotocin-induced diabetes increases the interaction of Bad/Bcl-XL and decreases the binding of pBad/14–3–3 in rat testis

Cited by 35 publications

References 27 publications

Enalapril reduces germ cell toxicity in streptozotocin-induced diabetic rat: investigation on possible mechanisms

Enalapril reduces germ cell toxicity in streptozotocin-induced diabetic rat: investigation on possible mechanisms

The effects of streptozotocin-induced diabetes on ghrelin expression in rat testis: biochemical and immunohistochemical study

MAPK immunoreactivity in streptozotocin-induced diabetic rat testis

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