Ameliorating diabetes-induced testicular dysfunction by modulating PKC/Nrf2/Bcl-2 signaling: Protective role of sulbutiamine

Biofactors. 2024 Jul-Aug;50(4):845-862. doi: 10.1002/biof.2046. Epub 2024 Feb 12.

Abstract

The prevalence of testicular dysfunction is increasing as it is a common diabetes mellites (DM) complication. The objective of this study is to explore the potential protective effect of sulbutiamine against testicular hypofunction associated with streptozotocin (STZ)-induced DM in rats. Sulbutiamine was administered orally (60 mg/kg) to male Wistar rats for 8 weeks starting 72 h after a single injection of STZ (45 mg/kg, i.p.). Blood glucose level (BGL), serum testosterone level, sperm number, and motility were determined. Testicular tissue was examined histopathologically, and the Johnson score was evaluated. Levels of malondialdehyde (MDA), protein kinase C (PKC), nuclear factor erythroid-derived 2-like 2 (Nrf2), and proliferating cell nuclear antigen (PCNA) were measured. Apoptosis was evaluated by immunohistochemical determination of B-cell lymphoma protein 2 (Bcl-2), Bcl-2 associated X-protein (Bax), and caspase-3. Sulbutiamine administration managed to reduce BGL and boost testicular function as manifested by increased testicular weight, testosterone level, sperm number, and motility compared to the STZ group. Additionally, histopathological examination revealed an improved histological picture and Johnson score of testicular tissue after sulbutiamine treatment. Sulbutiamine administration reduced testicular PKC, MDA, and PCNA levels and increased Nrf2 compared to the untreated group. Moreover, sulbutiamine treatment suppressed apoptosis triggered by STZ as evidenced by elevated Bcl-2, decreased Bax and reduced caspase-3. The present work revealed for the first time a promising protective role of sulbutiamine against STZ-induced testicular dysfunction which may add to the clinical utility of sulbutiamine. The underlying mechanisms involve reducing BGL and PKC, activating Nrf2 and inhibiting apoptosis.

Keywords: STZ; apoptosis; oxidative stress; sulbutiamine; testicular dysfunction.

MeSH terms

  • Animals
  • Apoptosis* / drug effects
  • Blood Glucose / drug effects
  • Blood Glucose / metabolism
  • Diabetes Mellitus, Experimental* / complications
  • Diabetes Mellitus, Experimental* / drug therapy
  • Diabetes Mellitus, Experimental* / metabolism
  • Male
  • Malondialdehyde / metabolism
  • NF-E2-Related Factor 2* / metabolism
  • Oxidative Stress / drug effects
  • Proliferating Cell Nuclear Antigen / metabolism
  • Protein Kinase C* / metabolism
  • Proto-Oncogene Proteins c-bcl-2* / genetics
  • Proto-Oncogene Proteins c-bcl-2* / metabolism
  • Rats
  • Rats, Wistar*
  • Signal Transduction* / drug effects
  • Streptozocin
  • Testicular Diseases / chemically induced
  • Testicular Diseases / drug therapy
  • Testicular Diseases / etiology
  • Testicular Diseases / metabolism
  • Testicular Diseases / pathology
  • Testicular Diseases / prevention & control
  • Testis* / drug effects
  • Testis* / metabolism
  • Testis* / pathology
  • Testosterone / blood

Substances

  • NF-E2-Related Factor 2
  • Proto-Oncogene Proteins c-bcl-2
  • Protein Kinase C
  • Nfe2l2 protein, rat
  • Testosterone
  • Malondialdehyde
  • Proliferating Cell Nuclear Antigen
  • Bcl2 protein, rat
  • Blood Glucose
  • Streptozocin