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Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway
المؤلفون المشاركون
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
المصدر
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-03-10
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1133545
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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