Cisplatin (CIS) is one of the widely used anticancer drugs. Despite its high efficiency in the treatment of testicular cancer, CIS has severe adverse effects on spermatogenesis and may even lead to infertility. Propolis is a honeybee product. It has free-radical scavenging activity.Aim
To evaluate the possible protective effect of bee propolis on CIS-induced testicular damage in adult male albino rats using histological, immunohistochemical, and morphometric studies.Materials and methods
Twenty-four adult male albino rats were divided into four groups, each group including six rats: control, propolis (100 mg/kg, orally daily for 7 days), CIS (10 mg/kg by a single intraperitoneal injection and left for 5 days without treatment), and combined therapy (propolis 7 days before CIS injection and continued for 5 days after). Testicular weights were measured. Histological (using H&E and Masson’s trichrome stains) and immunohistochemical [using nuclear factor-κB (NF-κB)/p65 and claudin 11] studies were carried out. Morphometric measurements of seminiferous tubule diameter, area% of collagen fibers, and claudin 11, in addition to the optical density of NF-κB/p65, were carried out, followed by statistical analysis.Results
Testicular weight decreased significantly in the CIS group. CIS induced distorted seminiferous tubules, cellular disorganization, wide separation of intertubular space, cytoplasmic vacuolation, and pyknotic nuclei. Increased area% of collagen fibers, increased optical density of NF-κB/p65 immunoreactivity, and decreased area% of claudin 11 immunoexpression were found in the spermatogenic cells. The combined therapy group showed a significant reduction in histological, immunohistochemical, and morphometric changes.Conclusions
A significant role of NF-κB activation was found in CIS-induced testicular damage. Blockade of NF-κB activation by propolis could be an effective strategy for protection from CIS-induced testicular damage, provided it is administered orally early enough before the administration of CIS. It also prevented the disruption of tight junction protein, claudin 11; thus, it could preserve blood–testis barrier function.