@article{MAKHILLRJBS202015611529,
    title = {Protective Activity of Dexamethasone Against Cycloposphamide-Induced Nephrotoxicity in
Rats},
    journal = {Research Journal of Biological Sciences},
    volume = {15},
    number = {6},
    pages = {130-137},
    year = {2020},
    issn = {1815-8846},
    doi = {rjbsci.2020.130.137},
    url = {https://makhillpublications.co/view-article.php?issn=1815-8846&doi=rjbsci.2020.130.137},
    author = {Elias},
    keywords = {Cyclophosphamide,kidney,toxicity,dexamethasone,rat},
    abstract = {The nephrotoxic effect of cyclophosphamide
(CP) may involve inflammation. Dexamethasone (DEXA)
is a glucocorticoid used for the treatment of inflammatory
disorders. This study examined the protective potential of
dexamethosane (DEXA) against CP-induced
nephrotoxicity in albino rats. Thirty-six adult male albino
rats divided in to six groups (n = 6) were used. Group I
(Control) was treated with normal saline (0.2 mL day<sup>&#150;1</sup>)
intraperitoneally (i.p.) for 24 h. Group 2 was treated with
DEXA (1 mg/kg/day i.p.) for 24 h. Group 3 was
treated with CP (150 mg/kg/day i.p.) for 24 h. Group 4
was pre-treated with DEXA (1 mg/kg/day) for 24 h before
treatment with CP (150 mg/kg/day i.p.) for 24 h. Group 5
was co-treated with DEXA (1 mg/kg/day i.p.) and
CP (150 mg/kg/day i.p.) ip for 24 h. Group 6 was treated
with CP (150 mg/kg/day i.p.) for 24 h before posttreatment
with DEXA (1 mg/kg/day i.p.) for 24 h. At the
termination of treatments, the rats were euthanized and
blood samples were assessed for serum renal function
markers. Kidney samples were evaluated for histology,
malondialdehyde and antioxidants (glutathione, catalase,
superoxide dismutase and glutathione peroxidase).
Treatment with CP produced significant (p<0.001)
increases in serum uric acid, creatinine, urea and kidney
malondialdehyde levels with significant (p<0.001)
decreases in serum albumin, total protein and kidney
antioxidants in relation to control. CP caused tubular
necroses and increased Bowman&#146;s space in the kidneys of
treated rats. CP-induced nephrotoxicity was significantly
abrogated by post-treatment (p<0.05), co-treatment
(p<0.01) and pre-treatment (p<0.001) with DEXA when
compared to CP. DEXA may be effective against
nephrotoxicity caused by CP.}
    }