Tags

Type your tag names separated by a space and hit enter

The cytoprotective effect of isorhamnetin against oxidative stress is mediated by the upregulation of the Nrf2-dependent HO-1 expression in C2C12 myoblasts through scavenging reactive oxygen species and ERK inactivation.
Gen Physiol Biophys. 2016 Apr; 35(2):145-54.GP

Abstract

This study was designed to confirm the protective effects of isorhamnetin against oxidative stress-induced cellular damage. Our results indicated that isorhamnetin inhibited the hydrogen peroxide (H2O2)-induced growth inhibition and exhibited scavenging activity against the intracellular reactive oxygen species (ROS) in mouse-derived C2C12 myoblasts. Isorhamnetin also significantly attenuated H2O2-induced DNA damage and apoptosis, and increased the levels of the nuclear factor erythroid 2-related factor 2 (Nrf2) and its phosphorylation associated with the induction of heme oxygenase-1 (HO-1). However, the protective effects of isorhamnetin on H2O2-induced ROS and growth inhibition were significantly abolished by an HO-1 competitive inhibitor. Moreover, the potential of isorhamnetin to mediate HO-1 induction and protect against H2O2-mediated growth inhibition was abrogated by transient transfection with Nrf2-specific small interfering RNA. Additionally, isorhamnetin induced the activation of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. However, the specific inhibitor of ERK, but not JNK and p38 MAPK, was able to abolish the HO-1 upregulation and the Nrf2 phosphorylation. Collectively, these results demonstrate that isorhamnetin augments the cellular antioxidant defense capacity by activating the Nrf2/HO-1 pathway involving the activation of the ERK pathway, thus protecting the C2C12 cells from H2O2-induced cytotoxicity.

Authors+Show Affiliations

Department of Biochemistry, Dongeui University College of Korean Medicine, 52-57, Yangjeong-ro, Busanjin, Busan 614-052, Republic of Korea. choiyh@deu.ac.kr.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26830132

Citation

Choi, Yung Hyun. "The Cytoprotective Effect of Isorhamnetin Against Oxidative Stress Is Mediated By the Upregulation of the Nrf2-dependent HO-1 Expression in C2C12 Myoblasts Through Scavenging Reactive Oxygen Species and ERK Inactivation." General Physiology and Biophysics, vol. 35, no. 2, 2016, pp. 145-54.
Choi YH. The cytoprotective effect of isorhamnetin against oxidative stress is mediated by the upregulation of the Nrf2-dependent HO-1 expression in C2C12 myoblasts through scavenging reactive oxygen species and ERK inactivation. Gen Physiol Biophys. 2016;35(2):145-54.
Choi, Y. H. (2016). The cytoprotective effect of isorhamnetin against oxidative stress is mediated by the upregulation of the Nrf2-dependent HO-1 expression in C2C12 myoblasts through scavenging reactive oxygen species and ERK inactivation. General Physiology and Biophysics, 35(2), 145-54. https://doi.org/10.4149/gpb_2015034
Choi YH. The Cytoprotective Effect of Isorhamnetin Against Oxidative Stress Is Mediated By the Upregulation of the Nrf2-dependent HO-1 Expression in C2C12 Myoblasts Through Scavenging Reactive Oxygen Species and ERK Inactivation. Gen Physiol Biophys. 2016;35(2):145-54. PubMed PMID: 26830132.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The cytoprotective effect of isorhamnetin against oxidative stress is mediated by the upregulation of the Nrf2-dependent HO-1 expression in C2C12 myoblasts through scavenging reactive oxygen species and ERK inactivation. A1 - Choi,Yung Hyun, Y1 - 2016/02/02/ PY - 2015/06/19/received PY - 2015/08/11/accepted PY - 2016/2/3/entrez PY - 2016/2/3/pubmed PY - 2016/7/13/medline SP - 145 EP - 54 JF - General physiology and biophysics JO - Gen Physiol Biophys VL - 35 IS - 2 N2 - This study was designed to confirm the protective effects of isorhamnetin against oxidative stress-induced cellular damage. Our results indicated that isorhamnetin inhibited the hydrogen peroxide (H2O2)-induced growth inhibition and exhibited scavenging activity against the intracellular reactive oxygen species (ROS) in mouse-derived C2C12 myoblasts. Isorhamnetin also significantly attenuated H2O2-induced DNA damage and apoptosis, and increased the levels of the nuclear factor erythroid 2-related factor 2 (Nrf2) and its phosphorylation associated with the induction of heme oxygenase-1 (HO-1). However, the protective effects of isorhamnetin on H2O2-induced ROS and growth inhibition were significantly abolished by an HO-1 competitive inhibitor. Moreover, the potential of isorhamnetin to mediate HO-1 induction and protect against H2O2-mediated growth inhibition was abrogated by transient transfection with Nrf2-specific small interfering RNA. Additionally, isorhamnetin induced the activation of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. However, the specific inhibitor of ERK, but not JNK and p38 MAPK, was able to abolish the HO-1 upregulation and the Nrf2 phosphorylation. Collectively, these results demonstrate that isorhamnetin augments the cellular antioxidant defense capacity by activating the Nrf2/HO-1 pathway involving the activation of the ERK pathway, thus protecting the C2C12 cells from H2O2-induced cytotoxicity. SN - 0231-5882 UR - https://www.unboundmedicine.com/medline/citation/26830132/The_cytoprotective_effect_of_isorhamnetin_against_oxidative_stress_is_mediated_by_the_upregulation_of_the_Nrf2_dependent_HO_1_expression_in_C2C12_myoblasts_through_scavenging_reactive_oxygen_species_and_ERK_inactivation_ L2 - http://www.aepress.sk/_downloads/dl.php?from=pubmed&journal=GPB&file=2016_02_145.pdf DB - PRIME DP - Unbound Medicine ER -