A comparative study on the cardiopulmonary protective effect of propolis versus coenzyme Q10 on paclitaxel-induced toxicity

Paclitaxel (PTX) is one of the most commercially and clinically effective chemotherapeutics, but its toxicity causes significant problems with its administration.  Consequently, it was intended in the current research to explore the potential activity of coenzyme Q10 (CoQ10) and propolis against PTX-induced cardiopulmonary damage. Thirty male albino rats were divided equally into six groups: control group; given saline, CoQ10 group; given CoQ10 (100 mg/kg b.wt daily), propolis group; given propolis (200 mg/kg b.wt daily), PTX group; given PTX (7.5 mg/kg b.wt i.p.), CoQ10+PTX group; given CoQ10 (100 mg/kg b.wt daily) before PTX (7.5 mg/kg b.wt) and propolis+PTX group; given propolis (200 mg/kg b.wt) before PTX (7.5 mg/kg b.wt). All treatments were received for 4 weeks. The PTX group had significantly higher serum concentrations of CK-MB and LDH. This result was concomitant with histopathological changes that represented by cardiac necrosis and degeneration together with congestion, edema and hemorrhage in the heart. Lung injury induced by PTX was characterized by perivascular hemorrhage, inflammatory cell infiltrates, bronchiolestenosis, hyperplasia and/or desquamation of the bronchiolar epithelium, alveolar emphysema, congestion, interstitial edema and fibrinoid necrosis of blood vessels walls. Besides, pulmonary fibrosis was confirmed by Van Gieson stain. Immunohistochemical staining for IL-1β revealed positive immunoexpression in heart and lung tissue. Treatment with CoQ10 and propolis ameliorated the cardiopulmonary toxicity induced by PTX indicated by improved microscopic picture of heart and lungs, serum biochemical parameters and decrease IL-1β immunoreactivity in heart and lung tissues. In conclusion, CoQ10 could be the best choice to counteract the cardiopulmonary toxicity produced by PTX exposure.