Roles of Fas/FasL-mediated apoptosis and inhibin B in the testicular dysfunction of rats with left-side varicocele.

We investigated the role of the Fas/FasL signalling pathway and inhibin B expression in rats with an experimentally induced left-side varicocele. Forty-five Sprague Dawley (SD) male rats were randomly divided into three groups in average: control group, sham group and experimental group. The expression of inhibin B in the rat left testis was analysed at the mRNA and protein levels by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting respectively. The expressions of Fas, FasL and caspase-3 in the left testis were measured by RT-PCR and immunofluorescence. The apoptosis index (AI) was measured by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Both the mRNA and protein of inhibin B were significantly reduced in the experimental group compared with that in the control group or the sham group. The expression of Fas, FasL and caspase-3 in the experimental group was significantly increased compared to that in the control group or the sham group. The concentration of serum inhibin B was also inversely related to circulating FSH concentrations and positively correlated with sperm count. It is concluded that Fas/FasL system may play an important role in apoptosis of rats with experimental varicocele and inhibin B could reflect spermatogenesis function.

[Relationship between decreased expression of inhibin B and spermatogenesis dysfunction in rats testis].

Objective: To explore the effects of varicocele on the expressions of inhibin B in rat testes and the relationship between expression of inhibin B and spermatogenesis dysfunction. Methods: Twenty specific-pathogen-free Sprague-Dawley (SD) male rats were randomly divided into two groups with random number table: 4-week control group (C4) and 4-week experimental group(V4). Experimental varicocele was created by partial ligation of left renal vein in the V4 group; vein isolation without ligation was performed in the C4 group.Spermatogenetic function in the two groups were assessed. The expression of inhibin B in the rat testis was analyzed by immunohistochemistry, the expressions of inhibin B, Fas and Fas ligand(FasL)mRNA measured by reverse transcription-polymerase chain reaction(RT-PCR), and the inhibin B protein expression by Western blot. Results: In comparison of spermatogenetic function in left rat testes, the Johnsen scores in the V4 group were significantly lower than those in the C4 group (9.79±0.05 vs 9.97±0.02, P=0.023), the seminiferous epithelium in the V4 group was significantly thinner than that in the C4 group [(48.35±0.99)µm vs (57.58±1.98)µm, P=0.000], and the number of sperms in the left epididymis was significantly lower than in the right one in the V4 group [(933±161)×106/(ml·g) vs(1 552±184)×106/(ml·g), P=0.017]. Both Western blot and immunohistochemical assay showed that the expression of inhibin B in the rat testes was significantly lower in the V4 group than in the C4 group(0.407±0.053 vs 0.608±0.076, P=0.038; 0.161±0.004 vs 0.183±0.005, P=0.008). RT-PCR also detected reduced expression of inhibin B mRNA in the V4 group compared with the C4 group(0.522±0.050 vs 1.106±0.210, P=0.003. Compared to the C4 group, the expression of Fas mRNA in the V4 group was significantly lower, while the expression of FasL mRNA in the V4 group was significantly higher(P=0.019, 0.015). Conclusions: Varicocele can lead to decreased expressions of inhibin B in rat testes and cause spermatogenesis dysfunction. There may be a close correlation between down-regulation ofinhibin B expression and spermatogenesis dysfunction.Inhibin B may play a significant rolein the mechanisms underlying male infertility due to varicocele.

Role of interleukin-6 gene polymorphisms in the development of prostate cancer.

We investigated the role of two functional polymorphisms, IL-6-174G>C (rs1800795) and IL-6-572C>G (rs1800796), in the development of prostate cancer. A total of 212 consecutive primary prostate cancer patients and 236 control subjects were recruited between May 2012 and May 2014. The IL-6-174G>C (rs1800795) and IL-6-572C>G (rs1800796) polymorphisms were assessed by polymerase chain reaction-restriction fragment length polymorphism. The genotype distributions of IL-6-174G>C (rs1800795) and IL-6-572C>G (rs1800796) met the Hardy-Weinberg equilibrium in the controls. Unconditional logistic regression analyses showed that the GG genotype of IL-6-572C>G (rs1800796) was associated with an elevated risk of prostate cancer compared with the CC genotype, and the OR (95%CI) for the GG genotype was 2.06 (1.11-3.87). In conclusion, we suggest that the IL-6-572C>G (rs1800796) gene polymorphism influences the development of prostate cancer.