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Effect of Cyclophosphamide on the Rat Urinary Bladder and the Possible Protective Role of Thymoquinone
Author(s) -
Sabry Hassan Sherif M.,
AlEyd Ghaith,
Thomann Charity,
Ahmad Zulfiqar
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.899.2
Subject(s) - thymoquinone , malondialdehyde , pharmacology , lipid peroxidation , cyclophosphamide , oxidative stress , nigella sativa , toxicity , medicine , glutathione , hemorrhagic cystitis , urinary system , intraperitoneal injection , catalase , chemistry , antioxidant , chemotherapy , biochemistry , traditional medicine , enzyme
Background Cyclophosphamide (CP) is a chemotherapeutic agent used for treating many neoplastic disease. Its application is limited now‐a‐days due to its multiple side effects including hemorrhagic cystitis. Thymoquinone (TQ) is one of the active ingredients of Nigella sativa seeds, known for its healing potentials. Aim of study The current study has been carried out to examine the protective effect of 2 different doses of TQ against CP‐induced oxidative injury in the urinary bladder in rat. In addition to the possible mechanism through which TQ produces its protective effect. Methods 5 groups of 40 rats were used in this study. An untreated control group receiving no treatment, a sham control group where TQ (10 mg/kg/day) was administered using gastric gavage, in a single oral dose for 10 consecutive days. A toxicity group where CP‐induced toxicity was induced via 100 mg/kg, intraperitoneal for 2 days. In addition to 2 protection groups, both receiving CP at a dose of 100 mg/kg, intraperitoneal for 2 days but receiving 2 different doses of TQ, at concentrations of 10 mg/kg/day for 10 days and 100 mg/kg/day for 5 days. Results CP caused alteration of the urinary bladder histology in rat, with significant oxidative stress (ROS), as revealed by the reduction in the catalase (CA) and glutathione reductase (GR) in blood, in addition to increased lipid peroxidation to compensate for the ROS as revealed by the increase in the malondialdehyde levels (MDA) in blood. CP also induced cell death, as revealed by the activation of caspase‐3 in blood. Post treatment with TQ (at a dose of 100mg/kg/day for 5 consecutive days), however reduced CP‐induced ROS and apoptosis. Conclusion Concomitant use of TQ with CP could ameliorate the CP‐induced toxicity on the rat urinary bladder via its antioxidant and antiapoptotic effects. Support or Funding Information Self Fund