The Protective Effects of Sesamin against Cyclophosphamide-Induced Nephrotoxicity through Modulation of Oxidative Stress, Inflammatory-Cytokines and Apoptosis in Rats

The Protective Effects of Sesamin against Cyclophosphamide-Induced Nephrotoxicity through Modulation of Oxidative Stress, Inflammatory-Cytokines and Apoptosis in Rats

Cyclophosphamide is an anticancer drug with a wide spectrum of clinical uses, but its typical side effects are multiple complications, including nephron toxicity. The possible molecular mechanism of the nephroprotective action of sesamin (SM) against cyclophosphamide (CP) induced renal toxicity was...

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Published in:International journal of molecular sciences Vol. 23; no. 19; p. 11615
Main Authors: Alshahrani, Saeed, Ali Thubab, Hani M., Ali Zaeri, Abdulrahman M., Anwer, Tarique, Ahmed, Rayan A., Jali, Abdulmajeed M., Qadri, Marwa, Nomier, Yousra, Moni, Sivakumar S., Alam, Mohammad F.
Format: Journal Article
Language:English
Published: Basel MDPI AG 01-10-2022
MDPI
Subjects:
Antioxidants
Apoptosis
Cancer therapies
Caspase-3
Chemotherapy
Creatinine
Cyclophosphamide
Cytokines
Drug dosages
Enzymes
Free radicals
IL-1β
Inflammation
inflammatory cytokines
Kidneys
Lipid peroxidation
Lipids
Liver
Metabolism
Metabolites
nephroprotective
Oxidative stress
Pathogenesis
Physiology
Seeds
sesamin
Toxicity
Tumor necrosis factor-α
Uric acid
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Summary:Cyclophosphamide is an anticancer drug with a wide spectrum of clinical uses, but its typical side effects are multiple complications, including nephron toxicity. The possible molecular mechanism of the nephroprotective action of sesamin (SM) against cyclophosphamide (CP) induced renal toxicity was investigated in rats by understanding oxidative stress and inflammatory cytokines. In this study, rats were arbitrarily grouped into the following four groups: a normal control group (CNT); a CP-induced toxicity group; a treatment group with two doses of sesamin SM10 and SM20; a group with sesamin (SM20) alone. A single dose of CP (150 mg/kg body, i.p.) was administered on day 4 of the experiments, while treatment with SM was given orally for seven days from day 1. The group treated with SM showed a significant protective effect against CP-induced renal damage in rats. Treatment with SM significantly increased the antioxidant enzymes (GSH, CAT, and SOD) and reduced malondialdehyde (MDA) levels. Thus, SM significantly overcame the elevated kidney function markers (creatinine, blood urea nitrogen, and uric acid) by attenuating oxidative stress. The SM also significantly reduced the elevated cytokines (IL-1β and TNFα) and caspase-3 in the treated group. Histopathological studies confirmed the protective effect of sesamin (SM) on CP-induced nephrotoxicity. In conclusion, the current findings support the nephroprotective effect of sesamin against CP-induced renal injury.
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content type line 23
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms231911615