Masoud Fallah Rajabpour Zare1, Kamran Rakhshan2, Nahid Aboutaleb3, Farnaz Nikbakht1, Nasim Naderi4, Morteza Bakhshesh5, Yaser Azizi6. 1. Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. 2. Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran. 3. Physiology Research Center and Department of Physiology, Iran University of Medical Sciences, Tehran, Iran. 4. Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran. 5. Khomein University of Medical Sciences, Khomein, Iran. 6. Physiology Research Center and Department of Physiology, Iran University of Medical Sciences, Tehran, Iran. Electronic address: azizi.y@iums.ac.ir.
Abstract
AIMS: Doxorubicin, an antibiotic belonging to anthracycline family, has been used for treatment of malignancies. Cardiotoxicity is the main adverse effect of doxorubicin. Apigenin, as a flavonoid, has antioxidant, anti-inflammatory and anti-tumoral properties. The aim of this study was the assessment of any protective effect of apigenin on cardiotoxicity induced by doxorubicin. MAIN METHODS: 40 male Wistar rats were randomly divided into 4 groups: control, cardiotoxicity (DOX), apigenin treated group (DOX + Api 25) and apigenin group (Api 25). At the end of the experiment, the markers of cardiac function (%EF, %FS, LVIDs, LVIDd), cardiac and liver injury (LDH, CK-MB, cTn-I, ALT, and AST), cardiac apoptosis (Bax, Bcl-2 and Caspase3), cardiac oxidative stress (SOD, GSH, MDA) and cardiac fibrosis were measured. KEY FINDINGS: Apigenin improved cardiac functional parameters. The levels of cardiac and liver injury markers were significantly decreased in DOX + Api 25 compared to DOX. Treatment with apigenin caused significant decrease in percentage of cardiac fibrosis in comparison with DOX. Apigenin in DOX + Api 25 group led to significant decrease in apoptotic proteins (Casp3, Bax) and a significant increase in anti-apoptotic proteins (Bcl2). In apigenin treatment groups, SOD levels significantly increased while a significant decrease was observed in MDA. The amount of GSH in DOX + Api 25 had no significant change in comparison to control and Api 25 groups. SIGNIFICANCE: Apigenin reduced cardiac injuries induced by DOX through anti-fibrotic, antioxidant and anti-apoptotic properties. It seems that apigenin prevents cardiac injuries and improves cardiac function.
AIMS: Doxorubicin, an antibiotic belonging to anthracycline family, has been used for treatment of malignancies. Cardiotoxicity is the main adverse effect of doxorubicin. Apigenin, as a flavonoid, has antioxidant, anti-inflammatory and anti-tumoral properties. The aim of this study was the assessment of any protective effect of apigenin on cardiotoxicity induced by doxorubicin. MAIN METHODS: 40 male Wistar rats were randomly divided into 4 groups: control, cardiotoxicity (DOX), apigenin treated group (DOX + Api 25) and apigenin group (Api 25). At the end of the experiment, the markers of cardiac function (%EF, %FS, LVIDs, LVIDd), cardiac and liver injury (LDH, CK-MB, cTn-I, ALT, and AST), cardiac apoptosis (Bax, Bcl-2 and Caspase3), cardiac oxidative stress (SOD, GSH, MDA) and cardiac fibrosis were measured. KEY FINDINGS:Apigenin improved cardiac functional parameters. The levels of cardiac and liver injury markers were significantly decreased in DOX + Api 25 compared to DOX. Treatment with apigenin caused significant decrease in percentage of cardiac fibrosis in comparison with DOX. Apigenin in DOX + Api 25 group led to significant decrease in apoptotic proteins (Casp3, Bax) and a significant increase in anti-apoptotic proteins (Bcl2). In apigenin treatment groups, SOD levels significantly increased while a significant decrease was observed in MDA. The amount of GSH in DOX + Api 25 had no significant change in comparison to control and Api 25 groups. SIGNIFICANCE: Apigenin reduced cardiac injuries induced by DOX through anti-fibrotic, antioxidant and anti-apoptotic properties. It seems that apigenin prevents cardiac injuries and improves cardiac function.
Authors: Marwa M M Refaie; Sayed Shehata; Randa Ahmed Ibrahim; Asmaa M A Bayoumi; Seham A Abdel-Gaber Journal: Cardiovasc Toxicol Date: 2021-09-11 Impact factor: 3.231
Authors: Heba A Elnoury; Salwa A Elgendy; Samar H Baloza; Heba I Ghamry; Mohamed Soliman; Eman Abdel-Mohsen Abdel-Aziz Journal: Toxicol Res (Camb) Date: 2022-06-20 Impact factor: 2.680
Authors: Nonhlakanipho F Sangweni; Derick van Vuuren; Lawrence Mabasa; Kwazi Gabuza; Barbara Huisamen; Sharnay Naidoo; Reenen Barry; Rabia Johnson Journal: Front Cardiovasc Med Date: 2022-06-22