Minocycline can reduce testicular apoptosis related to varicocele in male rats

Abstract

The current research aimed to assess the impacts of Minocycline on varicoceleinduced 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.

Evaluation of Expression of Cytochrome P450 Aromatase and Inflammatory, Oxidative, and Apoptotic Markers in Testicular Tissue of Obese Rats (Pre)Treated with Garlic Powder

“…Te testicular tissues and spermatozoa are very vulnerable to ROS attack and lipid peroxidation [8][9][10]. ROS produced by free fatty acids attack the cell membrane and cause damage to DNA and DNA fragmentation, which activates signaling pathways inducing testicular cell apoptosis [11][12][13]. Te fndings of the studies showed that ROS stimulated lipid peroxidation in the germ cell membrane and induced apoptosis in these cells [7,12,13].…”

Protective effects of an aqueous extract of Protaetia brevitarsis seulensis larvae against radiation‐induced testicular injury in mice

“…However, naturally occurring endogenous antioxidative systems (i.e., enzymatic and nonenzymatic antioxidants) protect against radiation‐induced oxidative damage by scavenging free radicals. Several studies have been reported on the association between antioxidant activity and testicular damages (Moghimian et al, 2017 ; Majid Shokoohi et al, 2022 ; Shokoohi et al, 2020 ; Soltani et al, 2018 ).…”

The evaluation of citral effects on experimental unilateral testicular ischemia/reperfusion injury

“…Following TT correction, more damage is done to the testicular tissue undergoing reperfusion injury than at the time of ischemia induction including tissue atrophy, disruption of seminiferous tubules, testosterone production reduction, fertility reduction, spermatogenesis reduction, and coagulative necrosis and disorganisation in germinal cell epithelium (Fehér & Bajory, 2016; Ünsal et al, 2006). Accumulation of ROS in ischemia/reperfusion (I/R) injury leads to DNA damage, lipid peroxidation, disorganisation in cell structure, protein coagulation, reduction in testosterone production, and activation of the germ cell apoptotic process (Shokoohi et al, 2020, 2022). Although the ischemic injury is an inevitable event, the complications of reperfusion should be prevented.…”