Publications by authors named "Maral Ramez"

4 Publications

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Conductive carbon nanofibers incorporated into collagen bio-scaffold assists myocardial injury repair.

Int J Biol Macromol 2020 Nov 2;163:1136-1146. Epub 2020 Jul 2.

Physiology Research Centre, Iran University of Medical Sciences, Tehran, Iran. Electronic address:

Currently, treatment of myocardial infarction considered as unmet clinical need. Nanomaterials have been used in the regeneration of tissues such as bone, dental and neural tissue in the body and have increased hope for revitalizing of damaged tissues. Conductive carbon base nanomaterials with its superior physicochemical properties have emerged as promising materials for cardiovascular application. In this study, we applied a biosynthetic collagen scaffold containing carbon nanofiber for regenerating of damaged heart tissue. The collagen-carbon nanofiber scaffold was fabricated and fully characterised. The scaffold was grafted on the affected area of myocardial ischemia, immediately after ligation of the left anterior descending artery in the wistar rat's model. After 4 weeks, histological analyses were performed for investigation of formation of immature cardio-myocytes, epicardial cells, and angiogenesis. Compared to untreated hearts, this scaffold significantly protects heart tissue against injury. This improvement is accompanied by a reduction in fibrosis and the increased formation of a blood vessel network and immature cardio-myocytes in the infarction heart. No toxicity detected with apoptotic and TUNEL assays. In conclusion, the mechanical support of the collagen scaffold with carbon nanofiber enhanced the regeneration of myocardial tissue.
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http://dx.doi.org/10.1016/j.ijbiomac.2020.06.259DOI Listing
November 2020

High-intensity interval training increases myocardial levels of Klotho and protects the heart against ischaemia-reperfusion injury.

Exp Physiol 2020 04 17;105(4):652-665. Epub 2020 Mar 17.

Department of Exercise physiology, Faculty of Physical Education and Sport Sciences, Kharazmi University, Tehran, Iran.

New Findings: What is the central question of this study? Can short-term high-intensity interval training (HIIT) contribute to the reduction of ischaemia-reperfusion (IR) injury by enhancing the levels of Klotho and its related axes, including myocardial TRPC6 expression, and antioxidant defence as novel possible mechanisms of exercise-induced cadioprotection (EICP) against IR injury? What is the main finding and its importance? The increase of plasma and myocardial levels of Klotho as a result of preconditioning with HIIT and prevention of a significant reduction of Klotho during IR injury can promote cardioprotection and reduce damage by attenuating myocardial TRPC6 expression and increasing antioxidant defence. The present findings may provide a new mechanism in EICP and IR injury, and provide the knowledge to develop preventive and therapeutic approaches.

Abstract: Cardiovascular disease, especially coronary artery disease, remains a major cause of morbidity and mortality in the world, and ischaemia-reperfusion (IR) insult is the main pathological cause leading to death. Exercise training is associated with a reduced risk of cardiovascular disease and the development of cardioprotection against IR injury. Therefore, the purpose of this study was to investigate the effect of preconditioning with high-intensity interval training (HIIT) on myocardial and plasma levels of Klotho and its related axes as novel mechanisms of exercise-induced cardioprotection against IR injury. Seventy male Wistar rats were randomly divided into five groups of control, HIIT, sham, IR and HIIT group that underwent IR injury (H-IR). The training group performed five sessions of HIIT on the treadmill. The cardiac IR injury was induced by ligation of the left anterior descending coronary artery for 30 min followed by 24 h reperfusion. Infarct size and histopathological assessment of cardiac tissues were determined through Evans Blue-triphenyltetrazolium chloride and haematoxylin-eosin staining, respectively. We investigated lipid peroxidation and markers of cardiac injury, antioxidant enzymes and the plasma levels of Klotho using enzyme-linked immunosorbent assays. Also, myocardial levels of Klotho and TRPC6 expression were determined by western blot assays. The results demonstrated a significant increase in myocardial and plasma levels of Klotho following HIIT and a significant decrease during IR injury. Myocardial TRPC6 channel expression increased following IR. HIIT also prevented a significant reduction of Klotho during IR and consequently reduced the expression of the TRPC6 channel in the H-IR group compared with the IR group. Furthermore, HIIT decreased the infarct size, cardiac injury, lipid peroxidation, lactate dehydrogenase, creatine kinase myocardial band and cardiac troponin-I, and improved total antioxidant capacity and catalase, superoxide dismutase and glutathione peroxidase activities following IR injury. The findings of the present study suggest that HIIT improves cardioprotection against IR injury and reduces cardiac damages through an increase in myocardial and plasma levels of Klotho and its related axes (TRPC6 and antioxidant defence). These findings can help to develop preventive and therapeutic approaches.
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http://dx.doi.org/10.1113/EP087994DOI Listing
April 2020

The effect of preconditioning with high-intensity training on tissue levels of G-CSF, its receptor and C-kit after an acute myocardial infarction in male rats.

BMC Cardiovasc Disord 2020 02 11;20(1):75. Epub 2020 Feb 11.

Physiology Research Center and Physiology Department, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Background: Exercise training is known as a practical way to increase cardioprotection against stress, and it seems that stem cell recruitment is one of its mechanisms. The purpose of the present study was to investigate the effect of preconditioning with High-intensity interval training (HIIT) on tissue levels of G-CSF, its receptor and C-Kit following acute myocardial infarction in male rats.

Methods: Twenty Male Wistar rats were randomly divided into 4 groups of control, MI, HIIT, and HIIT+MI. Training groups performed 2 weeks of high intensity interval training in 4 sections. The first section consisted training in 3 days and 2 sessions in each day (4 × 2 min with 35-40 m/min and 3 × 2 min with 25-30 m/min between high intervals. The second part included 2 days of training (4 × 2 min with 40 to 45 m/min and 3 × 2 min with 28 to 32 m /min). The third part was performed in 3 days with one more repetition. The fourth section consisted 2 days of training and with one more repetition compared to section 3. For induction of myocardial infarction, subcutaneous injection of isoprenaline was used. CK, total CK, LDH, and troponin T were measured in serum and G-CSF, G-CSFR and C-Kit proteins were measured by the Western Blot method in the heart tissue.

Results: The results of this study showed that enzymes of CK, total CK, LDH, troponin T had a significant increase in both MI and HIIT+MI groups compared to the other two groups (P < 0.001) and these indices in the MI group were significantly higher than the HIIT+MI group. Also, the results demonstrated that G-CSF, G-CSFR and C-Kit protein expression in the heart tissue significantly increased after MI. As well as, 2 weeks of HIIT training significantly increased G-CSF and C-kit in the training group compared to the control group, but the training caused that these proteins does not increase in HIIT+MI group as much as MI group.

Conclusions: Along with other protective pathways, high intensity interval training can increase cardioprotection and decrease heart injuries through the increase in G-CSF, G-CSFR and C-kit level.
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http://dx.doi.org/10.1186/s12872-020-01380-wDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7011373PMC
February 2020

The greater effect of high-intensity interval training versus moderate-intensity continuous training on cardioprotection against ischemia-reperfusion injury through Klotho levels and attenuate of myocardial TRPC6 expression.

BMC Cardiovasc Disord 2019 05 16;19(1):118. Epub 2019 May 16.

Physiology Research Center and Physiology Department, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Background: Myocardial ischemia-reperfusion (IR) injury is a leading cause of death all over the world, so developing practical approaches to promote cardioprotection against IR injury is essential. Exercise training is an effective strategy to improve cardioprotection. Hence, the purpose of this study was to investigate the effect of short-term preconditioning with two types of high-intensity interval training (HIIT) and moderate intensity continuous training (MICT) on klotho and TRPC6 mechanisms in cardioprotection.

Methods: Eighty Male Wistar rats (250-300 g) were randomly divided into 7 groups, including Control, HIIT, MICT, Sham, IR, HIIT+IR, and MICT+IR. Training was performed in 5 consecutive days. HIIT protocol consisted of running on the treadmill at intervals 85-90% vomax that separated by slow intensity periods at 50-60% vomax. MICT program was performed at 70% VOmax at the same running distance with HIIT groups. The cardiac IR injury was induced by LAD occlusion followed by reperfusion. ELISA kit was used in order to measure the plasma levels of klotho, LDH and CK-MB, and TRPC6 expression was determined using the western blot technique. Data were analyzed using one way ANOVA and Tukey's post hoc tests.

Results: The results of this study showed that both types of exercise training programs significantly increase plasma levels of klotho and reduce the infarct size and heart injury. In addition, the exercise training decreased the amount of TRPC6 channels expression during IR. However, the effect of HIIT on increasing the klotho and cardioprotection was greater compared to MICT.

Conclusions: Based on the results, even a short-term of aerobic exercise training, especially HIIT, promotes cardioprotection against IR injury and decreases infarct size via an increase in klotho and attenuate of protein expression of myocardial TRPC6 during IR.
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http://dx.doi.org/10.1186/s12872-019-1090-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6524218PMC
May 2019