Possible protective effect of royal jelly against cyclophosphamide induced prostatic damage in male albino rats; a biochemical, histological and immuno-histo-chemical study

Anti-Cancer and Protective Effects of Royal Jelly for Therapy-Induced Toxicities in Malignancies

“…Furthermore, it was also reported that RJ decreased the tissue content of MDA, which was increased by an anti-cancer agent, in the lung tissue of rats treated with bleomycin [ 43 ]. The GSH-Px level in the prostate was significantly higher in rats administered with cyclophosphamide and RJ than those administered cyclophosphamide only [ 51 ] and similar findings was also reported in the lung of rats treated with bleomycin [ 43 ]. In rats treated by MTX, the plasma MDA levels in the MTX and RJ-treated group were significantly lower than those in the MTX-treated group and the plasma levels of SOD and GSH-Px in the MTX and RJ-treated group were higher than those in MTX-treated group [ 52 ].…”

“…Cyclophosphamide is a cytotoxic alkylating agent that it is often used for the treatment of cancer. In a rat model, RJ showed significant protective effects against cyclophosphamide-induced prostate cancer damage [ 51 ] and oral RJ administration to rats protected against the histological damage to the small intestine induced by methotrexate (MTX), which has anti-cancer effects via folate antagonist activity [ 52 ]. In short, mucosal thickness, villus length, villus length/crypt ratio and semi-quantitative histological evaluation in rats treated with MTX was significantly difference to those treated with MTX and RJ [ 52 ].…”

“…In addition, such protective effects observed in the small intestine after 100 mg/kg RJ administration were higher than those after 50 mg/kg administration [ 52 ]. These two different studies showed that part of the protective effects in the prostate and small intestine was potentially associated with the regulation of oxidative stress [ 51 , 52 ].…”

“…In contrast, the same study showed that the reactivity of Bcl-xL, which is an inhibitor of apoptosis, was lower in the kidney and liver of rats treated with CDDP than in control rats and that this decrease in reactivity was restored in rats treated with CDDP and RJ [ 47 ]. Other investigators have reported that cyclophosphamide increased the expression of Bax, which is a stimulator of apoptosis, in most of the prostatic acini of rats; however, the cyclophosphamide-induced change in Bax expression was improved by the concomitant administration of CDDP and RJ [ 51 ]. In addition, this study showed that although CP led to marked morphological changes, such as cystic dilatation with lost papillary fold in acini, flattened lining epithelium, wall integrity and apparent rupture of some acini, these changes of pathological features were suppressed by RJ via the modulation of Bax immunoreactivity [ 51 ].…”

“…In the endothelial cells of rat prostate tissues, eNOS expression in the cyclophosphamide and RJ-treated group was significantly lower than that in cyclophosphamide group [ 51 ]. Unfortunately, the relationship between such changes and anti-cancer agent-induced toxicities in normal tissues is not well characterized.…”