Oxidative status and chymotrypsin-like activity in right and left ventricle hypertrophy in an experimental model of emphysema

Tonon, Jair; Guarnier, Flávia Alessandra; Brunnquell, Cláudia Roberta; Bernardes, Sara Santos; Cecchini, Alessandra Lourenço; Cecchini, Rúbens

doi:10.1016/j.pathophys.2013.08.003

Cited by 3 publications

(3 citation statements)

References 41 publications

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“…Oxidative stress plays a critical role in the pathogenesis of cardiac hypertrophy (23,26,34). 5-ALA is endogenous in animals and is the first compound produced in the heme biosynthetic pathway via 5-ALA synthase (11).…”

Section: Discussionmentioning

confidence: 99%

5-Aminolevulinic acid combined with sodium ferrous citrate ameliorates H₂O₂-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway

Zhao

Guo

Chen

et al. 2015

American Journal of Physiology-Cell Physiology

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Hydrogen peroxide (H2O2) causes cell damage via oxidative stress. Heme oxygenase-1 (HO-1) is an antioxidant enzyme that can protect cardiomyocytes against oxidative stress. In this study, we investigated whether the heme precursor 5-aminolevulinic acid (5-ALA) with sodium ferrous citrate (SFC) could protect cardiomyocytes from H2O2-induced hypertrophy via modulation of HO-1 expression. HL-1 cells pretreated with/without 5-ALA and SFC were exposed to H2O2 to induce a cardiomyocyte hypertrophy model. Hypertrophy was evaluated by planar morphometry, (3)H-leucine incorporation, and RT-PCR analysis of hypertrophy-related gene expressions. Reactive oxygen species (ROS) production was assessed by 5/6-chloromethyl-2',7'-ichlorodihydrofluorescein diacetate acetylester. HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf2) protein expressions were analyzed by Western blot. In our experiments, HL-1 cells were transfected with Nrf2 siRNA or treated with a signal pathway inhibitor. We found several results. 1) ROS production, cell surface area, protein synthesis, and expressions of hypertrophic marker genes, including atrial natriuretic peptide, brain natriuretic peptide, atrial natriuretic factor, and β-myosin heavy chain, were decreased in HL-1 cells pretreated with 5-ALA and SFC. 2) 5-ALA and SFC increased HO-1 expression in a dose- and time-dependent manner, associated with upregulation of Nrf2. Notably, Nrf2 siRNA dramatically reduced HO-1 expression in HL-1 cells. 3) ERK1/2, p38, and SAPK/JNK signaling pathways were activated and modulate 5-ALA- and SFC-enhanced HO-1 expression. SB203580 (p38 kinase), PD98059 (ERK), or SP600125 (JNK) inhibitors significantly reduced this effect. In conclusion, our data suggest that 5-ALA and SFC protect HL-1 cells from H2O2-induced cardiac hypertrophy via activation of the MAPK/Nrf2/HO-1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

5-Aminolevulinic acid combined with sodium ferrous citrate ameliorates H₂O₂-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway

Zhao

Guo

Chen

et al. 2015

American Journal of Physiology-Cell Physiology

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“…Cardiac hypertrophy is a complex inflammatory disease that develops via the dysregulation of various signal transduction pathways and oxidative stress and excess ROS production and plays a definitive role in the pathogenicity of cardiac hypertrophy [75][76][77]. Using HL-1 cells, a murine cardiomyocyte cell line that maintains phenotypic characteristics of adult cardiomyocytes [78], and a well-established in vitro model of oxidant-induced cardiomyocyte hypertrophy [79], we evaluated the protective effect of 5-ALA/SFC on cardiac hypertrophy (unpublished data).…”

Section: Cardiomyocyte Hypertrophymentioning

confidence: 99%

“…Using HL-1 cells, a murine cardiomyocyte cell line that maintains phenotypic characteristics of adult cardiomyocytes [78], and a well-established in vitro model of oxidant-induced cardiomyocyte hypertrophy [79], we evaluated the protective effect of 5-ALA/SFC on cardiac hypertrophy (unpublished data). Numerous studies have indicated that intrinsic antioxidants, including superoxide dismutase and vitamin E, can remit hypertrophy through the reduction of ROS generation [77,80,81]. Additionally, simvastatin, a reductase inhibitor, can function as an antioxidant and inhibit hypertrophy via the inhibition of ROS production [82].…”

Section: Cardiomyocyte Hypertrophymentioning

confidence: 99%

5-Aminolevulinic acid regulates the inflammatory response and alloimmune reaction

Fujino

Nishio

Ito

et al. 2016

International Immunopharmacology

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5-Aminolevulinic acid (5-ALA) is a naturally occurring amino acid and precursor of heme and protoporphyrin IX (PpIX). Exogenously administrated 5-ALA increases the accumulation of PpIX in tumor cells specifically due to the compromised metabolism of 5-ALA to heme in mitochondria. PpIX emits red fluorescence by the irradiation of blue light and the formation of reactive oxygen species and singlet oxygen. Thus, performing a photodynamic diagnosis (PDD) and photodynamic therapy (PDT) using 5-ALA have given rise to a new strategy for tumor diagnosis and therapy. In addition to the field of tumor therapy, 5-ALA has been implicated in the treatment of inflammatory disease, autoimmune disease and transplantation due to the anti-inflammation and immunoregulation properties that are elicited with the expression of heme oxygenase (HO)-1, an inducible enzyme that catalyzes the rate-limiting step in the oxidative degradation of heme to free iron, biliverdin and carbon monoxide (CO), in combination with sodium ferrous citrate (SFC), because an inhibitor of HO-1 abolishes the effects of 5-ALA. Furthermore, NF-E2-related factor 2 (Nrf2), mitogen-activated protein kinase (MAPK), and heme are involved in the HO-1 expression. Biliverdin and CO are also known to have anti-apoptotic, anti-inflammatory and immunoregulatory functions. We herein review the current use of 5-ALA in inflammatory diseases, transplantation medicine, and tumor therapy.

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Pulmonary Emphysema Impairs Male Reproductive Physiology Due To Testosterone and Oxidative Stress Imbalance in Mesocricetus auratus

et al. 2020

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Oxidative status and chymotrypsin-like activity in right and left ventricle hypertrophy in an experimental model of emphysema

Cited by 3 publications

References 41 publications

5-Aminolevulinic acid combined with sodium ferrous citrate ameliorates H₂O₂-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway

5-Aminolevulinic acid combined with sodium ferrous citrate ameliorates H₂O₂-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway

5-Aminolevulinic acid regulates the inflammatory response and alloimmune reaction

Pulmonary Emphysema Impairs Male Reproductive Physiology Due To Testosterone and Oxidative Stress Imbalance in Mesocricetus auratus

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Oxidative status and chymotrypsin-like activity in right and left ventricle hypertrophy in an experimental model of emphysema

Cited by 3 publications

References 41 publications

5-Aminolevulinic acid combined with sodium ferrous citrate ameliorates H2O2-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway

5-Aminolevulinic acid combined with sodium ferrous citrate ameliorates H2O2-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway

5-Aminolevulinic acid regulates the inflammatory response and alloimmune reaction

Pulmonary Emphysema Impairs Male Reproductive Physiology Due To Testosterone and Oxidative Stress Imbalance in Mesocricetus auratus

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Product

Resources

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5-Aminolevulinic acid combined with sodium ferrous citrate ameliorates H₂O₂-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway

5-Aminolevulinic acid combined with sodium ferrous citrate ameliorates H₂O₂-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway