This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Cardiometabolic disorders (CMD) are a cluster of metabolic derangements that increases the susceptibility to insulin resistance and type II diabetes mellitus, systemic hypertension, central obesity, and dyslipidaemia [1, 2]. The rise in the prevalence of CMD is a global phenomenon involving developed nations and underdeveloped and developing countries, leading to a double burden of disease in the tropics. CMD is a multifactorial disorder caused by an intricate interaction between genetics and environmental factors, which lead to increased insulin resistance and circulatory free fatty acids (FFA), lipid and glucose dysmetabolism, and elevated levels of adipokines and cytokines [1, 3–7].
Studies have linked OS with incident CMD [8]. The observed dwindling antioxidant level in advanced age has been shown to reduce cardiotolerance [9]. This is accompanied by arterial thickening, atherosclerosis, vascular damage, and remodeling [10, 11]. These contribute to the development of CMD. Indepth knowledge of the impact of OS in the development of CMD will help to identify possible effective treatment modalities to improve cardiometabolic status.
The purpose of this special issue is to illuminate the effect of OS in the etiopathogenesis of CMD and open new management opportunities. This special issue, oxidative stress and cardiometabolic disorders, contains contributions from 34 reputable scientists from 17 different institutions across the globe.
The first article, “Orosomucoid 1 Attenuates Doxorubicin-Induced OS and Apoptosis in Cardiomyocytes via Nrf2 Signaling,” by X. Cheng et al. documents the rescue effect of orosomucid 1 on doxorubicin-induced cardiotoxicity. The authors clearly demonstrated that orosomucid 1, an acute-phase protein, attenuated inflammation and ischemic stroke in an animal model via upregulation of nuclear factor-like 2 (Nrf2) and suppression of heme oxygenase 1 (HO-1) [12]. In addition, there was a reversal of the impact of ORM1 on doxorubicin-induced OS and apoptosis in cardiac muscles when Nrf2 was silenced. Their study lends credence to the use of orosomucid as a therapeutic strategy for doxorubicin-induced cardiotoxicity.
In the second article, “The Free Radical Scavenging and Anti-Isolated Human LDL Oxidation Activities of Pluchea indica (L.) Less. Tea Compared to Green Tea (Camellia sinensis),” K. Sirichaiwetchakoon et al. challenged isolated human low-density lipoproteins (LDL) with either 2,2
N. Zhao et al., in the third article, “Role of Oxidation-Dependent CaMKII Activation in the Genesis of Abnormal Action Potentials in Atrial Cardiomyocytes: A Simulation Study,” probed the influence of oxidation-dependent Ca2+/calmodulin-dependent protein kinase II (CaMKII) activation in the genesis of abnormal atrial action potentials (AP) [18]. Zhao and his colleagues explored the intrinsic pathophysiology of OS-induced arrhythmia in the atria. They observed that OS triggered early after depolarizations of AP by modifying the dynamics of transmembrane currents and intracellular calcium cycling. OS caused a rise in cytoplasmic calcium ions via enhancement of L-type Ca2+ current and calcium release by the sarcoplasmic reticulum. The resultant increases in intracellular calcium level, elevated Na+/Ca2+ exchange current, and reduced repolarization of the action potential. This culminated in prolonged AP and consequent early after depolarizations.
The study in the fourth article “Qiliqiangxin Improves Cardiac Function through Regulating Energy Metabolism via HIF-1α-Dependent and Independent Mechanisms in Heart Failure Rats after Acute Myocardial Infarction,” authored by Y. Wang et al. was designed to evaluate the influence of Qiliqiangxin, QL, on energy metabolism in experimental myocardial infarction and the role of hypoxia-inducible factor 1α (HIF-1α) signaling [19]. Acute myocardial infarction (AMI) was established by ligating the left anterior descending coronary artery in adult male Sprague Dawley rats, and animals with an
The fifth article, “Dracocephalum moldavica L. Extracts Protect H9c2 Cardiomyocytes against H2O2-Induced Apoptosis and OS,” evaluated the cardioprotective potential of Dracocephalum moldavica L., a phytomedicinal plant used in the management of cardiovascular diseases in China against H2O2-induced apoptosis and OS in H9c2 cells. M. Jin et al. pretreated H9c2 cells with Dracocephalum moldavica L. before challenging with H2O2 [20]. Dracocephalum moldavica L. therapy was found to attenuate H2O2-induced decline in cell viability, SOD activity, and mitochondrial membrane potential. The phenol- and flavonoid-rich Dracocephalum moldavica L. also abrogated H2O2-induced elevations in ROS generation and concentrations of MDA and lactate dehydrogenase. Dracocephalum moldavica L. cardioprotective activities were revealed to be mediated through upregulation of the Bcl-2 expression and downregulation of the Bax and caspase 3 expression.
In the sixth article, “Multimodal α-Glucosidase and α-Amylase Inhibition and Antioxidant Effect of the Aqueous and Methanol Extracts from the Trunk Bark of Ceiba pentandra,” T.B. Nguelefack et al. explored the postprandial modulatory activities and antioxidant potentials of Ceiba pentandra aqueous and methanolic stem bark extracts [21]. They demonstrated that the phenol- and flavonoid-rich extracts of Ceiba pentandra significantly reduced postprandial hyperglycemia by inhibiting protein oxidation, α-amylase, and α-glucosidase through scavenging reactive oxygen species. These findings are extensions of their previous studies that revealed that Ceiba pentandra promotes glucose utilization and reduces hepatic glucose release [22], upregulates glycogen synthesis, and impairs gluconeogenesis [23], inhibits lipid peroxidation and shows antioxidant activity against DPPH and hydroxyl radical [22], and demonstrated antidiabetic properties in dexamethasone-treated rats [24] and high-fat diet/streptozotocin-treated rats [25].
We hope our readers will find these articles interesting and stimulating. The articles and recommendations of the contributing experts will hopefully spur further discussion and expand research in these biomedical areas.
[1] S. M. Grundy, J. I. Cleeman, S. R. Daniels, K. A. Donato, R. H. Eckel, B. A. Franklin, D. J. Gordon, R. M. Krauss, P. J. Savage, Smith SC Jr, J. A. Spertus, F. Costa, American Heart Association, National Heart, Lung, and Blood Institute, "Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement," Circulation, vol. 112 no. 17, pp. 2735-2752, DOI: 10.1161/CIRCULATIONAHA.105.169404, 2005.
[2] R. Akhigbe, A. Ajayi, "The impact of reactive oxygen species in the development of cardiometabolic disorders: a review," Lipids in Health and Disease, vol. 20 no. 1,DOI: 10.1186/s12944-021-01435-7, 2021.
[3] K. Esposito, F. Giugliano, E. Martedi, G. Feola, R. Marfella, M. D'Armiento, D. Giugliano, "High proportions of erectile dysfunction in men with the metabolic syndrome," Diabetes Care, vol. 28 no. 5, pp. 1201-1203, DOI: 10.2337/diacare.28.5.1201, 2005.
[4] R. E. Akhigbe, L. O. Ajayi, A. F. Ajayi, "Codeine exerts cardiorenal injury via upregulation of adenine deaminase/xanthine oxidase and caspase 3 signaling," Life Sciences, vol. 273,DOI: 10.1016/j.lfs.2020.118717, 2021.
[5] N. Méndez-Sánchez, N. C. Chavez-Tapia, D. Motola-Kuba, K. Sanchez-Lara, G. Ponciano-Rodríguez, H. Baptista, M. H. Ramos, M. Uribe, "Metabolic syndrome as a risk factor for gallstone disease," World Journal of Gastroenterology, vol. 11 no. 11, pp. 1653-1657, DOI: 10.3748/wjg.v11.i11.1653, 2005.
[6] A. F. Ajayi, R. E. Akhigbe, L. O. Ajayi, "Activation of cardiac TNF- α in altered thyroid state-induced cardiometabolic disorder," Journal of Cardiovascular Disease Research, vol. 8 no. 4, pp. 151-156, DOI: 10.5530/jcdr.2017.4.33, 2017.
[7] S. F. Ige, R. E. Akhigbe, "Common onion (_Allium cepa_) extract reverses cadmium-induced organ toxicity and dyslipidaemia via redox alteration in rats," Pathophysiology, vol. 20 no. 4, pp. 269-274, DOI: 10.1016/j.pathophys.2013.04.002, 2013.
[8] M. A. Hamed, G. O. Aremu, R. E. Akhigbe, "Concomitant administration of HAART aggravates anti-Koch-induced oxidative hepatorenal damage via dysregulation of glutathione and elevation of uric acid production," Biomedicine and Pharmacotherapy, vol. 137,DOI: 10.1016/j.biopha.2021.111309, 2021.
[9] P. Abete, C. Napoli, G. Santoro, N. Ferrara, I. Tritto, M. Chiariello, F. Rengo, G. Ambrosio, "Age-related decrease in cardiac tolerance to oxidative stress," Journal of Molecular and Cellular Cardiology, vol. 31 no. 1, pp. 227-236, DOI: 10.1006/jmcc.1998.0862, 1999.
[10] T. E. Brinkley, B. J. Nicklas, A. M. Kanaya, S. Satterfield, E. G. Lakatta, E. M. Simonsick, K. Sutton-Tyrrell, S. B. Kritchevsky, "Plasma oxidized low-density lipoprotein levels and arterial stiffness in older adults," Hypertension, vol. 53 no. 5, pp. 846-852, DOI: 10.1161/HYPERTENSIONAHA.108.127043, 2009.
[11] D. Gradinaru, C. Borsa, C. Ionescu, G. I. Prada, "Oxidized LDL and NO synthesis--biomarkers of endothelial dysfunction and ageing," Mechanisms of Ageing and Development, vol. 151, pp. 101-113, DOI: 10.1016/j.mad.2015.03.003, 2015.
[12] X. Cheng, D. Liu, R. Xing, H. Song, X. Tian, C. Yan, Y. Han, "Orosomucoid 1 Attenuates Doxorubicin-Induced Oxidative Stress and Apoptosis in Cardiomyocytes via Nrf2 Signaling," BioMed Research International, vol. 2020,DOI: 10.1155/2020/5923572, 2020.
[13] K. Sirichaiwetchakoon, G. M. Lowe, G. Eumkeb, "The free radical scavenging and anti-isolated human LDL oxidation activities of Pluchea indica (L.) Less. Tea compared to green tea (Camellia sinensis)," BioMed Research International, vol. 2020,DOI: 10.1155/2020/4183643, 2020.
[14] L. K. Leung, Y. Su, R. Chen, Z. Zhang, Y. Huang, Z. Y. Chen, "Theaflavins in black tea and catechins in green tea are equally effective antioxidants," The Journal of Nutrition, vol. 131 no. 9, pp. 2248-2251, DOI: 10.1093/jn/131.9.2248, 2001.
[15] C. Folch-Cano, C. Jullian, H. Speisky, C. Olea-Azar, "Antioxidant activity of inclusion complexes of tea catechins with β -cyclodextrins by ORAC assays," Food Research International, vol. 43 no. 8, pp. 2039-2044, DOI: 10.1016/j.foodres.2010.06.006, 2010.
[16] K. Yamagata, "Protective effect of epigallocatechin gallate on endothelial disorders in atherosclerosis," Journal of Cardiovascular Pharmacology, vol. 75 no. 4, pp. 292-298, DOI: 10.1097/FJC.0000000000000792, 2020.
[17] S. Kongkiatpaiboon, S. Chewchinda, B. Vongsak, "Optimization of extraction method and HPLC analysis of six caffeoylquinic acids in _Pluchea indica_ leaves from different provenances in Thailand," Revista Brasileira de Farmacognosia, vol. 28 no. 2, pp. 145-150, DOI: 10.1016/j.bjp.2018.03.002, 2018.
[18] N. Zhao, Q. Li, H. Sui, H. Zhang, "Role of oxidation-dependent CaMKII activation in the genesis of abnormal action potentials in atrial cardiomyocytes: a simulation study," BioMed Research International, vol. 2020,DOI: 10.1155/2020/1597012, 2020.
[19] Y. Wang, M. Fu, J. Wang, J. Zhang, X. Han, Y. Song, Y. Fan, K. Hu, J. Zhou, J. Ge, "Qiliqiangxin improves cardiac function through regulating energy metabolism via HIF-1 α -dependent and independent mechanisms in heart failure rats after acute myocardial infarction," BioMed Research International, vol. 2020,DOI: 10.1155/2020/1276195, 2020.
[20] M. Jin, H. Yu, X. Jin, L. Yan, J. Wang, Z. Wang, "Dracocephalum moldavica L. Extracts Protect H9c2 Cardiomyocytes against H2O2-Induced Apoptosis and Oxidative Stress," BioMed Research International, vol. 2020,DOI: 10.1155/2020/8379358, 2020.
[21] T. B. Nguelefack, C. K. Fofie, E. P. Nguelefack-Mbuyo, A. K. Wuyt, "Multimodal α -glucosidase and α -amylase inhibition and antioxidant effect of the aqueous and methanol extracts from the trunk bark of Ceiba pentandra," BioMed Research International, vol. 2020,DOI: 10.1155/2020/3063674, 2020.
[22] C. K. Fofie, S. L. Wansi, E. P. Nguelefack-Mbuyo, A. D. Atsamo, P. Watcho, A. Kamanyi, T. Nole, T. B. Nguelefack, "In vitro anti-hyperglycemic and antioxidant properties of extracts from the stem bark of Ceiba pentandra," Journal of Complementary and Integrative Medicine, vol. 11 no. 3, pp. 185-193, DOI: 10.1515/jcim-2014-0031, 2014.
[23] K. S. Fofie, K. S, Nguelefack-mbuyo, K. A, K. B, C. N, S. V, N. TB, "Insulin sensitizing effect as possible mechanism of the antidiabetic properties of the methanol and the aqueous extracts from the trunk bark of Ceiba pentandra," Diabetes Updates, vol. 5 no. 1,DOI: 10.15761/DU.1000114, 2018.
[24] C. K. Fofié, E. P. Nguelefack-Mbuyo, N. Tsabang, A. Kamanyi, T. B. Nguelefack, "Hypoglycemic properties of the aqueous extract from the stem bark of Ceiba pentandra in dexamethasone-induced insulin resistant rats," Evidence-based Complementary and Alternative Medicine, vol. 2018,DOI: 10.1155/2018/4234981, 2018.
[25] C. K. Fofie, S. Katekhaye, S. Borse, V. Sharma, M. Nivsarkar, E. P. Nguelefack-Mbuyo, A. Kamanyi, V. Singh, T. B. Nguelefack, "Antidiabetic properties of aqueous and methanol extracts from the trunk bark ofCeiba pentandrain type 2 diabetic rat," Cell Biochemistry, vol. 120 no. 7, pp. 11573-11581, DOI: 10.1002/jcb.28437, 2019.
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Abstract
The authors clearly demonstrated that orosomucid 1, an acute-phase protein, attenuated inflammation and ischemic stroke in an animal model via upregulation of nuclear factor-like 2 (Nrf2) and suppression of heme oxygenase 1 (HO-1) [12]. The study in the fourth article “Qiliqiangxin Improves Cardiac Function through Regulating Energy Metabolism via HIF-1α-Dependent and Independent Mechanisms in Heart Failure Rats after Acute Myocardial Infarction,” authored by Y. Wang et al. was designed to evaluate the influence of Qiliqiangxin, QL, on energy metabolism in experimental myocardial infarction and the role of hypoxia-inducible factor 1α (HIF-1α) signaling [19]. Acute myocardial infarction (AMI) was established by ligating the left anterior descending coronary artery in adult male Sprague Dawley rats, and animals with an ejection fraction<50% at two weeks postoperation were considered animals with heart failure. Roland E. AkhigbeAyodeji F. AjayiSahu K. Ram [1] S. M. Grundy, J. I. Cleeman, S. R. Daniels, K. A. Donato, R. H. Eckel, B. A. Franklin, D. J. Gordon, R. M. Krauss, P. J. Savage, Smith SC Jr, J. A. Spertus, F. Costa, American Heart Association, National Heart, Lung, and Blood Institute, "Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement," Circulation, vol. 112 no. 17, pp. 2735-2752, DOI: 10.1161/CIRCULATIONAHA.105.169404, 2005.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
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1 Reproductive Physiology and Bioinformatics Research Unit, Department of Physiology, College of Medicine, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria; Reproductive Biology and Toxicology Research Laboratories, Oasis of Grace Hospital, Osogbo, Osun State, Nigeria; Department of Chemical Sciences, Kings University, Ode Omu, Osun, Nigeria
2 Reproductive Physiology and Bioinformatics Research Unit, Department of Physiology, College of Medicine, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria
3 Department of Pharmaceutical Sciences, Assam University (A Central University), Silchar-788011 (AS), India