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      Aerobic training and L-arginine supplement attenuates myocardial infarction-induced kidney and liver injury in rats via reduced oxidative stress

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          Abstract

          Introduction

          The aim of the present study was to determine the effect of exercise training and l-arginine supplementation on kidney and liver injury in rats with myocardial infarction (MI).

          Material and methods

          Four weeks after MI, 50 male wistar rats randomly divided into five followed groups: sham surgery without MI (Sham, n = 10), Sedentary-MI (Sed-MI, n = 10) 3: L-Arginine-MI (La-MI, n = 10) 4: Exercise training-MI (Ex-MI, n = 10) and 5: Exercise and L-arginine-MI (Ex + La-MI). Ex-MI and Ex + La-MI groups running on a treadmill for 10 weeks with moderate intensity. Rats in the L-arginine-treated groups drank water containing 4% L-arginine. Tissues oxidative stress and kidney and liver functional indices were measured after treatments.

          Result

          Urea as a kidney function indexes, increased in Sed-MI group in compared to sham group and decreased significantly in Ex-MI and Ex + La-MI groups. The level of catalase (CAT) and glutathione stimulating hormone (GSH) of kidney were significantly lower in the MI-groups compared with the Sham group and kidney Malondialdehyde (MDA) levels increased after MI and significantly decreased in response to aerobic training and L-arginine. As well as, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) as liver injury indices, increased in MI-groups and decreased by training and L-arginine. In this regards, liver MDA and CAT respectively increased and decreased in MI-groups, but aerobic training and L-arginine increased liver glutathione per-oxidase (GPx) and decreased liver MDA.

          Conclusion

          These results demonstrated that kidney and liver function impaired 14 weeks after MI and aerobic training and L-arginine supplementation synergistically ameliorated kidneys and liver injury in myocardial infarction rats through oxidative stress reduction.

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          Most cited references36

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          Formation of malonaldehyde from phospholipid arachidonate during microsomal lipid peroxidation.

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            Heart diseases affecting the liver and liver diseases affecting the heart.

            The association of cardiac and liver disorders has not been extensively outlined in the literature. A survey of the MEDLINE database was performed to assess the current status of research regarding the association between cardiac and liver disorders. Combined cardiac and hepatic disorders occur in 3 different settings: heart diseases affecting the liver, liver diseases affecting the heart, and cardiac and hepatic disorders with joint etiology. The spectrum of heart diseases affecting the liver includes mild alterations of liver function tests in heart failure, cardiogenic ischemic hepatitis, congestive liver fibrosis, and cardiac cirrhosis. The liver diseases affecting the heart include complications of cirrhosis such as hepatopulmonary syndrome, portopulmonary hypertension, pericardial effusion, and cirrhotic cardiomyopathy as well as noncirrhotic cardiac disorders such as high-output failure caused by intrahepatic arteriovenous fistulae. Cardiac and hepatic disorders with joint etiology include infectious, metabolic, immune, vasculitic, and toxic disorders. We propose a practical approach to a diagnostic workup of combined cardiac and hepatic disorders based on recognizing the sequence of appearance of the cardiac and liver disease, presence of features of a multisystem disease, and presence of pathognomonic features. The evaluation of combined cardiac and hepatic disorders takes into consideration the expected benefit of treatment and the risks related to invasive procedures. Accordingly, investigations can be limited to ancillary tests for patients with congested liver and mild alterations of liver function tests, in cardiogenic ischemic hepatitis, patients with cardiac cirrhosis who are proposed for conservative treatment, and multisystem disease involving the heart and the liver. Conversely, comprehensive investigations are recommended when invasive therapeutic interventions are considered for the treatment of hepatopulmonary syndrome, portopulmonary hypertension, or arteriovenous fistulae. Classification of a patient to any of the 3 categories-heart diseases affecting the liver, liver diseases affecting the heart, and cardiac and hepatic disorders with joint etiology-permits the physician to narrow the span of the possible diagnoses and allows for a more simple workup.
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              Influence of exercise training and age on CD14+ cell-surface expression of toll-like receptor 2 and 4.

              The influence of an exercise training program and age on inflammatory cytokine production and CD14+cell-surface expression of toll-like receptor 2 (TLR2) and toll-like receptor 4 (TLR4) was examined in 60 younger and older subjects. Subjects were assigned to: young physically active (YPA, n = 15; 25.2 +/- 5.0 years), young physically inactive (YPI, n = 14; 24.9 +/- 4.7 years), older physically active (OPA, n = 14; 71.2 +/- 4.4 years) or older physically inactive (OPI, n = 17; 71.0 +/- 4.3 years) groups. YPI and OPI completed 12 weeks (3 days/week) of endurance (20 min) and resistance exercise (eight exercises, two sets). YPA and OPA groups were instructed to continue their normal activity for 12 weeks. Blood was collected at rest, before and after the 12-week training and control period. A whole blood method was used to determine lipopolysaccharide-(LPS) and peptidoglycan-(PGN) stimulated IL-6, IL-1beta, and TNF-alpha production with supernatants analyzed using ELISA. CD14+ cell-surface expression of TLR2 and TLR4 were measured using flow cytometry. Training increased estimated VO(2max) by 10.4% and increased strength by an average of 38.1%. YPI and OPI had a post-training reduction in LPS-stimulated IL-6 production (P < .01), but LPS-stimulated IL-1beta and TNF-alpha and PGN-stimulated cytokines were not changed. CD14+ cell TLR4 was significantly reduced (P < .05) in YPI and OPI groups after training, but TLR2 was not significantly changed. An exercise training program reduced LPS-stimulated IL-6, concomitant with lower TLR4. These results provide further support for a training- or physical activity-induced lowering of TLR4 and inflammation.
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                Author and article information

                Contributors
                Journal
                Indian Heart J
                Indian Heart J
                Indian Heart Journal
                Elsevier
                0019-4832
                Jul-Aug 2018
                30 August 2017
                : 70
                : 4
                : 538-543
                Affiliations
                [a ]Department of Physical Education and Sport Science, Bandar Abbas, Islamic Azad University, Bandar Abbas, Iran
                [b ]Department of Sport Physiology, Faculty of Physical Education and Sport Science, Bu Ali Sina University, Hamedan, Iran
                [c ]Student Research Committee, Lorestan University of Medical Sciences, Khorramabad, Iran
                [d ]Razi Herbal Medicines Research Center, Department of Physiology, Lorestan University of Medical Sciences, Khorramabad, Iran
                Author notes
                [* ]Corresponding author at: Herbal Medicines Research Center, Department of Physiology, Lorestan University of Medical Sciences, Khorramabad, Iran. nazari257@ 123456yahoo.com
                Article
                S0019-4832(16)30566-1
                10.1016/j.ihj.2017.08.011
                6116575
                30170650
                0d6552ab-0f5d-4adf-98fa-a886a7f652b1
                © 2017 Published by Elsevier B.V. on behalf of Cardiological Society of India.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 28 October 2016
                : 15 August 2017
                Categories
                Pre-clinical

                myocardial infarction,kidney and liver dysfunction,oxidative stress,aerobic training

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