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Gastrodin attenuation of the inflammatory response in H9c2 cardiomyocytes involves inhibition of NF-κB and MAPKs activation via the phosphatidylinositol 3-kinase signaling.
Biochem Pharmacol. 2013 Apr 15; 85(8):1124-33.BP

Abstract

The phenolic glucoside gastrodin, a main constituent of a Chinese traditional herbal medicine, has been known to display several biological and pharmacological properties. However, the role and precise molecular mechanisms explaining how gastrodin suppresses the inflammatory response in septic cardiac dysfunction are unknown. To study this, rat H9c2 cardiomyocytes were treated with gastrodin and/or lipopolysaccharide (LPS). Our results showed that gastrodin treatment strongly suppressed nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) family activation and upregulation of the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in LPS-stimulated H9c2 cardiomyocytes. Simultaneously, gastrodin obviously upregulated the phosphatidylinositol 3-kinase (PI3-K)/Akt signaling in a dose-dependent manner. However, wortmannin, a specific PI3-K inhibitor, blocked the inhibitory effects of gastrodin on LPS-stimulated H9c2 cardiomyocytes. Furthermore, PI3-K/Akt inhibition partially abolished the inhibitory effects of gastrodin on the phosphorylation of inhibitor κB-α (IκB-α), extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK), and activity of NF-κB. Here we report activation of the PI3-K/Akt signaling by gastrodin and that inhibition of this pathway reverses the inhibitory effects of gastrodin on NF-κB and MAPKs activation in H9c2 cardiomyocytes.

Authors+Show Affiliations

Department of Anatomy, Faculty of Basic Medical Sciences, Kunming Medical University, Kunming 650500, China. yangping19871022@gmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23376120

Citation

Yang, Ping, et al. "Gastrodin Attenuation of the Inflammatory Response in H9c2 Cardiomyocytes Involves Inhibition of NF-κB and MAPKs Activation Via the Phosphatidylinositol 3-kinase Signaling." Biochemical Pharmacology, vol. 85, no. 8, 2013, pp. 1124-33.
Yang P, Han Y, Gui L, et al. Gastrodin attenuation of the inflammatory response in H9c2 cardiomyocytes involves inhibition of NF-κB and MAPKs activation via the phosphatidylinositol 3-kinase signaling. Biochem Pharmacol. 2013;85(8):1124-33.
Yang, P., Han, Y., Gui, L., Sun, J., Chen, Y. L., Song, R., Guo, J. Z., Xie, Y. N., Lu, D., & Sun, L. (2013). Gastrodin attenuation of the inflammatory response in H9c2 cardiomyocytes involves inhibition of NF-κB and MAPKs activation via the phosphatidylinositol 3-kinase signaling. Biochemical Pharmacology, 85(8), 1124-33. https://doi.org/10.1016/j.bcp.2013.01.020
Yang P, et al. Gastrodin Attenuation of the Inflammatory Response in H9c2 Cardiomyocytes Involves Inhibition of NF-κB and MAPKs Activation Via the Phosphatidylinositol 3-kinase Signaling. Biochem Pharmacol. 2013 Apr 15;85(8):1124-33. PubMed PMID: 23376120.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gastrodin attenuation of the inflammatory response in H9c2 cardiomyocytes involves inhibition of NF-κB and MAPKs activation via the phosphatidylinositol 3-kinase signaling. AU - Yang,Ping, AU - Han,Yi, AU - Gui,Li, AU - Sun,Jun, AU - Chen,Yuan-li, AU - Song,Rui, AU - Guo,Jia-zhi, AU - Xie,Ya-nan, AU - Lu,Di, AU - Sun,Lin, Y1 - 2013/01/29/ PY - 2012/12/05/received PY - 2013/01/22/revised PY - 2013/01/23/accepted PY - 2013/2/5/entrez PY - 2013/2/5/pubmed PY - 2013/5/17/medline SP - 1124 EP - 33 JF - Biochemical pharmacology JO - Biochem Pharmacol VL - 85 IS - 8 N2 - The phenolic glucoside gastrodin, a main constituent of a Chinese traditional herbal medicine, has been known to display several biological and pharmacological properties. However, the role and precise molecular mechanisms explaining how gastrodin suppresses the inflammatory response in septic cardiac dysfunction are unknown. To study this, rat H9c2 cardiomyocytes were treated with gastrodin and/or lipopolysaccharide (LPS). Our results showed that gastrodin treatment strongly suppressed nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) family activation and upregulation of the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in LPS-stimulated H9c2 cardiomyocytes. Simultaneously, gastrodin obviously upregulated the phosphatidylinositol 3-kinase (PI3-K)/Akt signaling in a dose-dependent manner. However, wortmannin, a specific PI3-K inhibitor, blocked the inhibitory effects of gastrodin on LPS-stimulated H9c2 cardiomyocytes. Furthermore, PI3-K/Akt inhibition partially abolished the inhibitory effects of gastrodin on the phosphorylation of inhibitor κB-α (IκB-α), extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK), and activity of NF-κB. Here we report activation of the PI3-K/Akt signaling by gastrodin and that inhibition of this pathway reverses the inhibitory effects of gastrodin on NF-κB and MAPKs activation in H9c2 cardiomyocytes. SN - 1873-2968 UR - https://www.unboundmedicine.com/medline/citation/23376120/Gastrodin_attenuation_of_the_inflammatory_response_in_H9c2_cardiomyocytes_involves_inhibition_of_NF_κB_and_MAPKs_activation_via_the_phosphatidylinositol_3_kinase_signaling_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-2952(13)00057-9 DB - PRIME DP - Unbound Medicine ER -