Bahjat Al-Ani1, Norah M Alzamil2, Peter W Hewett3, Fahaid Al-Hashem1, Ismaeel Bin-Jaliah1, Abdullah S Shatoor4, Samaa S Kamar5, Noha S Abdel Latif6, Mohamed A Haidara7, Amal F Dawood7,8. 1. Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia. 2. Department of Clinical Science, Family Medicine, College of Medicine, Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia. 3. Institute of Cardiovascular Sciences, College of Medicine and Dental Sciences, University of Birmingham, Birmingham, UK. 4. Department of Internal Medicine, College of Medicine, King Khalid University, Abha, Saudi Arabia. 5. Departments of Medical Histology, Kasr al-Aini Faculty of Medicine, Cairo University, Cairo, Egypt. 6. Department of Medical Pharmacology, Kasr al-Aini Faculty of Medicine, Cairo University, Cairo, Egypt. 7. Department of Physiology, Kasr al-Aini Faculty of Medicine, Cairo University, Cairo, Egypt. 8. Department of Basic Medical Sciences, College of Medicine, Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia.
Abstract
BACKGROUND: The link between oxidative stress (ROS), apoptosis (p53) and fibrosis (collagen) in type 2 diabetes mellitus (T2DM)-induced cardiac injury in the presence and absence of the antidiabetic drug, metformin has not been investigated before. MATERIAL AND METHODS: T2DM was induced in rats by a combination of high carbohydrate and fat diets (HCFD) and streptozotocin (50 mg/kg) injection. The protection group started metformin (200 mg/kg) treatment 14 days prior to the induction of diabetes and continued on metformin and HCFD until being sacrificed at week 12. RESULTS: Diabetes significantly induced blood levels of ROS and left ventricular p53 and collagen expression that was inhibited by metformin. Metformin also significantly reduced glycated haemoglobin and dyslipidemia induced by diabetes. In addition, a significant correlation between ROS-p53-collagen axis and glycaemia and hyperlipidaemia was observed. CONCLUSIONS: These findings show that metformin provides substantial protection against diabetic cardiomyopathy-induced ROS-p53 mediated fibrosis and dyslipidemia.
BACKGROUND: The link between oxidative stress (ROS), apoptosis (p53) and fibrosis (collagen) in type 2 diabetes mellitus (T2DM)-induced cardiac injury in the presence and absence of the antidiabetic drug, metformin has not been investigated before. MATERIAL AND METHODS: T2DM was induced in rats by a combination of high carbohydrate and fat diets (HCFD) and streptozotocin (50 mg/kg) injection. The protection group started metformin (200 mg/kg) treatment 14 days prior to the induction of diabetes and continued on metformin and HCFD until being sacrificed at week 12. RESULTS: Diabetes significantly induced blood levels of ROS and left ventricular p53 and collagen expression that was inhibited by metformin. Metformin also significantly reduced glycated haemoglobin and dyslipidemia induced by diabetes. In addition, a significant correlation between ROS-p53-collagen axis and glycaemia and hyperlipidaemia was observed. CONCLUSIONS: These findings show that metformin provides substantial protection against diabetic cardiomyopathy-induced ROS-p53 mediated fibrosis and dyslipidemia.
Entities:
Keywords:
Diabetes; ROS-p53-collagen axis; cardiac injury; metformin; rat model
Authors: Amal F Dawood; Norah M Alzamil; Peter W Hewett; Maha A Momenah; Mohammad Dallak; Samaa S Kamar; Dina H Abdel Kader; Hanaa Yassin; Mohamed A Haidara; Amro Maarouf; Bahjat Al-Ani Journal: Biomedicines Date: 2022-04-23
Authors: Amal F Dawood; Amro Maarouf; Norah M Alzamil; Maha A Momenah; Ayed A Shati; Nervana M Bayoumy; Samaa S Kamar; Mohamed A Haidara; Asmaa M ShamsEldeen; Hanaa Z Yassin; Peter W Hewett; Bahjat Al-Ani Journal: Biomedicines Date: 2022-07-08
Authors: Amal F Dawood; Suliman Al Humayed; Maha A Momenah; Mohamed El-Sherbiny; Hend Ashour; Samaa S Kamar; Asmaa M ShamsEldeen; Mohamed A Haidara; Bahjat Al-Ani; Hasnaa A Ebrahim Journal: Diagnostics (Basel) Date: 2022-07-21