EXPERIMENTAL RESEARCH
Effect of thymoquinone on cyclophosphamide-induced injury in the rat urinary bladder
| 1 | Anatomy Department, Faculty of Medicine, Cairo University, Cairo, Egypt |
| 2 | Medical Physiology Department, Faculty of Medicine, Cairo University, Cairo, Egypt |
| 3 | Fielding Graduate University, Student-Doctor of Clinical Psychology |
| 4 | California University of Science and Medicine, School of Medicine, San Bernardino, California, USA |
| 5 | Department of Medical Education, California University of Science and Medicine, School of Medicine, San Bernardino, California, USA |
Submission date: 2019-10-25
Final revision date: 2020-04-23
Acceptance date: 2020-06-14
Online publication date: 2020-07-08
KEYWORDS
Oxidative stressprotectionthymoquinonecyclophosphamideUrinary bladderoxidative stressurinary bladder
TOPICS
ABSTRACT
Introduction:
Cyclophosphamide (CP) is a chemotherapeutic agent used to treat neoplastic diseases, but its side effects include hemorrhagic cystitis. Thymoquinone (TQ) is an active ingredient of Nigella sativa with healing potential. This study examined the protective effect of TQ against CP-induced oxidative injury in rat urinary bladder.
Material and methods:
Sixty rats were divided into 6 equal groups: untreated control (group A), TQ-treated with 10 mg/kg/day TQ for 10 days (group B1), TQ-treated with 100 mg/kg/day TQ for 5 days (group B2), toxicity control where 100 mg/kg CP was administered for 2 days (group C), CP + TQ-treated with the same TQ treatment as group B1 and 100 mg/kg CP for 2 days (group D1), and CP + TQ-treated with the same TQ treatment as group B2 and 100 mg/kg CP for 2 days (group D2). Rat urinary bladders were assessed histopathologically via hematoxylin and eosin (H&E) and Masson’s trichrome stains and were evaluated for oxidative stress and cell death markers.
Results:
CP demonstrated significant reduction in glutathione reductase, and increased malondialdehyde levels and protein carbonylation (both p < 0.05). CP also induced cell death as measured by caspase-3 activation. Pretreatment with TQ (group D2) reduced CP-induced oxidative stress and apoptosis.
Conclusions:
TQ may ameliorate CP-induced oxidative injury in rat urinary bladder, via its antioxidant and antiapoptotic effects.
Cyclophosphamide (CP) is a chemotherapeutic agent used to treat neoplastic diseases, but its side effects include hemorrhagic cystitis. Thymoquinone (TQ) is an active ingredient of Nigella sativa with healing potential. This study examined the protective effect of TQ against CP-induced oxidative injury in rat urinary bladder.
Material and methods:
Sixty rats were divided into 6 equal groups: untreated control (group A), TQ-treated with 10 mg/kg/day TQ for 10 days (group B1), TQ-treated with 100 mg/kg/day TQ for 5 days (group B2), toxicity control where 100 mg/kg CP was administered for 2 days (group C), CP + TQ-treated with the same TQ treatment as group B1 and 100 mg/kg CP for 2 days (group D1), and CP + TQ-treated with the same TQ treatment as group B2 and 100 mg/kg CP for 2 days (group D2). Rat urinary bladders were assessed histopathologically via hematoxylin and eosin (H&E) and Masson’s trichrome stains and were evaluated for oxidative stress and cell death markers.
Results:
CP demonstrated significant reduction in glutathione reductase, and increased malondialdehyde levels and protein carbonylation (both p < 0.05). CP also induced cell death as measured by caspase-3 activation. Pretreatment with TQ (group D2) reduced CP-induced oxidative stress and apoptosis.
Conclusions:
TQ may ameliorate CP-induced oxidative injury in rat urinary bladder, via its antioxidant and antiapoptotic effects.
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