Berberine protects against diclofenac sodium-induced testicular impairment in mice by its anti-oxidant and anti-apoptotic activities

This study was designed to investigate the effect of berberine (BBR) on diclofenac sodium-induced testicular impairment in mice.  Eighteen male mice were divided randomly and equally into three groups for three weeks. One group was kept as control, the second group was injected intraperitoneally with diclofenac sodium (DS) at a dose of 10 mg/kg BW daily during the second and third weeks. The third group received daily oral administration of BBR at a dose of 50 mg/kg BW throughout the whole period of the experiment in parallel with the injection of the above-mentioned dose of DS during the second and third weeks. Plasma testosterone as well as testicular lipid peroxides (LPO), nitric oxide (NO), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were evaluated. In paraffin-embedded testicular tissues, histological examination, immuno-expression of glutathione reductase (GR), and TUNEL assay were carried out.  Testosterone levels were within the normal range in all groups. BBR decreased testicular LPO and induced SOD and GSH without marked changes in CAT and NO. The histology of testis was improved and, regularity and integrity of seminiferous tubules basement membranes, and distribution and amount of peritubular collagen fibers were normalized. BBR treated group showed few positive GR immuno-expression in spermatogenic cells and negative GR immuno-expression in interstitial cells of Leydig along with a few apoptotic spermatogenic cells.  BBR is effective in protecting against DS-induced testicular dysfunction by improving oxidant/anti-oxidant balance and blocking the apoptotic cascade.