Minocycline can reduce testicular apoptosis related to varicocele in male rats.
Majid ShokoohiArash KhakiAyda Roudi Rasht AbadiLinda MohammadZadeh BoukaniSepideh Hassanpour KhodaieHossein KalarestaghiAmir Afshin KhakiMaryam MoghimianHamid Reza NiazkarHamed ShooreiPublished in: Andrologia (2022)
The current research aimed to assess the impacts of Minocycline on varicocele-induced regulation of apoptotic-related genes and oxidative stress in the testis of adult Wistar rats. Thirty-two rats were divided into 4 groups: sham, varicocele (VcI), varicocele treated with Minocycline (VcI + Mno) for 56 days and healthy rats treated with minocycline (Mno). After 8 weeks, the oxidative stress markers levels in serum were investigated, afterwards, the level of Bax and Bcl-2 expression were assessed through 'immunocytochemistry' and RT-qPCR assays. Also, the rate of apoptosis was evaluated through the TUNEL method. Johnson's score, 'the width of epithelium' and 'seminiferous tubules diameter' were ameliorated in the VcI + Mno group in comparison with the Vcl group. Administration of Minocycline raised the 'Glutathione peroxidase' and 'Superoxide dismutase' levels in serum and declined the Malondialdehyde level in serum (p = 0.001). Furthermore, current study represented that minocycline reduced Bax and enhanced the expression of Bcl-2 gene and protein in comparison with the Vcl group (p < 0.05). In addition, Minocycline administration significantly declined the rate of apoptosis in germ cells (p < 0.05). Our study demonstrated that the administration of Minocycline could improve testicular injury in varicocele-induced rats by its antioxidant activity.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- cell cycle arrest
- endoplasmic reticulum stress
- cell death
- poor prognosis
- dna damage
- ischemia reperfusion injury
- high glucose
- cell proliferation
- signaling pathway
- binding protein
- young adults
- germ cell
- hydrogen peroxide
- gene expression
- high throughput
- mass spectrometry
- stress induced
- heat shock
- heat stress
- childhood cancer
- heat shock protein