Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway
Joint Authors
Alkharfy, Khalid M.
Al-Jenoobi, F. I.
Ahad, Abdul
Ahmad, Ajaz
Bin Jardan, Yousef A.
Ansari, Mushtaq Ahmad
Raish, Mohammad
Haq, Nazrul
Khan, Mohd Rashid
Source
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-03-10
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Abstract EN
In the present study, we explored SA’s activity against DOX-induced cardiotoxicity and revealed its underlying mechanisms.
Male Wistar rats (weight, 190-210g; n=6) were randomly divided into four groups: group I, normal control; group II, DOX 15 mg/kg via intraperitoneal (ip) route; group III, administered DOX+SA 20 mg/kg; and group IV, administered DOX+captopril (CAP 30 mg/kg).
SA and CAP were administered orally for seven days, and DOX (15 mg/kg) was injected intraperitoneally an hour before SA treatment on the fifth day.
Forty-eight hours after DOX administration, animals were anesthetized and sacrificed for molecular and histology experiments.
SA significantly mitigated the myocardial effects of DOX, and following daily administration, it reduced serum levels of lactate dehydrogenase (LDH) and creatine kinase isoenzyme-MB to near normal values.
Levels of oxidative stress markers, glutathione-peroxidase, superoxide dismutase, and catalase, in the cardiac tissue were significantly increased, whereas malondialdehyde levels decreased after SA treatment in DOX-administered rats.
Furthermore, DOX caused an inflammatory reaction by elevating the levels of proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and endothelin- (ET-) 1, as well as nuclear factor kappa-B (NF-κB) expression.
Daily administration of SA significantly repressed TNF-α, IL-1β, ET-1, and NF-κB levels.
caspase-3 and Bax expression, bcl-2-like protein and caspase-3 activities and levels.
Overall, we found that SA could inhibit DOX-induced cardiotoxicity by inhibiting oxidative stress, inflammation, and apoptotic damage.
American Psychological Association (APA)
Bin Jardan, Yousef A.& Ansari, Mushtaq Ahmad& Raish, Mohammad& Alkharfy, Khalid M.& Ahad, Abdul& Al-Jenoobi, F. I.…[et al.]. 2020. Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway. BioMed Research International،Vol. 2020, no. 2020, pp.1-10.
https://search.emarefa.net/detail/BIM-1133545
Modern Language Association (MLA)
Bin Jardan, Yousef A.…[et al.]. Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway. BioMed Research International No. 2020 (2020), pp.1-10.
https://search.emarefa.net/detail/BIM-1133545
American Medical Association (AMA)
Bin Jardan, Yousef A.& Ansari, Mushtaq Ahmad& Raish, Mohammad& Alkharfy, Khalid M.& Ahad, Abdul& Al-Jenoobi, F. I.…[et al.]. Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-10.
https://search.emarefa.net/detail/BIM-1133545
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1133545