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Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways.
BMC Complement Altern Med. 2014 Jul 09; 14:233.BC

Abstract

BACKGROUND

Lysophosphatidylcholine (lysoPC), a metabolite from membrane phospholipids, accumulates in the ischemic myocardium and plays an important role in the development of myocardial dysfunction ventricular arrhythmia. In this study, we investigated if baicalein, a major component of Huang Qui, can protect against lysoPC-induced cytotoxicity in rat H9c2 embryonic cardiomyocytes.

METHODS

Cell viability was detected by the MTT assay; ROS levels were assessed using DCFH-DA; and intracellular free calcium concentrations were assayed by spectrofluorophotometer. Cell apoptosis and necrosis were evaluated by the flow cytometry assay and Hoechst staining. Mitogen-Activated Protein Kinases (MAPKs), which included the ERK, JNK, and p38, and the apoptotic mechanisms including Bcl-2/Bax, caspase-3, caspase-9 and cytochrome c pathways were examined by Western blot analysis. The activation of MAPKs was examined by enzyme-linked immunosorbent assay.

RESULTS

We found that lysoPC induced death and apoptosis of H9c2 cells in a dose-dependent manner. Baicalein could prevent lysoPC-induced cell death, production of reactive oxygen species (ROS), and increase of intracellular calcium concentration in H9c2 cardiomyoctes. In addition, baicalein also inhibited lysoPC-induced apoptosis, with associated decreased pro-apoptotic Bax protein, increased anti-apoptotic Bcl-2 protein, resulting in an increase in the Bcl-2/Bax ratio. Finally, baicalein attenuated lysoPC-induced the expression of cytochrome c, casapase-3, casapase-9, and the phosphorylations of ERK1/2, JNK, and p38. LysoPC-induced ERK1/2, JNK, and p38 activations were inhibited by baicalein.

CONCLUSIONS

Baicalein protects cardiomyocytes from lysoPC-induced apoptosis by reducing ROS production, inhibition of calcium overload, and deactivations of MAPK signaling pathways.

Authors+Show Affiliations

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. chchhs@kmu.edu.tw.No affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

25012390

Citation

Chen, Huai-Min, et al. "Baicalein, an Active Component of Scutellaria Baicalensis Georgi, Prevents Lysophosphatidylcholine-induced Cardiac Injury By Reducing Reactive Oxygen Species Production, Calcium Overload and Apoptosis Via MAPK Pathways." BMC Complementary and Alternative Medicine, vol. 14, 2014, p. 233.
Chen HM, Hsu JH, Liou SF, et al. Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways. BMC Complement Altern Med. 2014;14:233.
Chen, H. M., Hsu, J. H., Liou, S. F., Chen, T. J., Chen, L. Y., Chiu, C. C., & Yeh, J. L. (2014). Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways. BMC Complementary and Alternative Medicine, 14, 233. https://doi.org/10.1186/1472-6882-14-233
Chen HM, et al. Baicalein, an Active Component of Scutellaria Baicalensis Georgi, Prevents Lysophosphatidylcholine-induced Cardiac Injury By Reducing Reactive Oxygen Species Production, Calcium Overload and Apoptosis Via MAPK Pathways. BMC Complement Altern Med. 2014 Jul 9;14:233. PubMed PMID: 25012390.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways. AU - Chen,Huai-Min, AU - Hsu,Jong-Hau, AU - Liou,Shu-Fen, AU - Chen,Tsan-Ju, AU - Chen,Li-Ying, AU - Chiu,Chaw-Chi, AU - Yeh,Jwu-Lai, Y1 - 2014/07/09/ PY - 2013/11/15/received PY - 2014/05/14/accepted PY - 2014/7/12/entrez PY - 2014/7/12/pubmed PY - 2014/10/21/medline SP - 233 EP - 233 JF - BMC complementary and alternative medicine JO - BMC Complement Altern Med VL - 14 N2 - BACKGROUND: Lysophosphatidylcholine (lysoPC), a metabolite from membrane phospholipids, accumulates in the ischemic myocardium and plays an important role in the development of myocardial dysfunction ventricular arrhythmia. In this study, we investigated if baicalein, a major component of Huang Qui, can protect against lysoPC-induced cytotoxicity in rat H9c2 embryonic cardiomyocytes. METHODS: Cell viability was detected by the MTT assay; ROS levels were assessed using DCFH-DA; and intracellular free calcium concentrations were assayed by spectrofluorophotometer. Cell apoptosis and necrosis were evaluated by the flow cytometry assay and Hoechst staining. Mitogen-Activated Protein Kinases (MAPKs), which included the ERK, JNK, and p38, and the apoptotic mechanisms including Bcl-2/Bax, caspase-3, caspase-9 and cytochrome c pathways were examined by Western blot analysis. The activation of MAPKs was examined by enzyme-linked immunosorbent assay. RESULTS: We found that lysoPC induced death and apoptosis of H9c2 cells in a dose-dependent manner. Baicalein could prevent lysoPC-induced cell death, production of reactive oxygen species (ROS), and increase of intracellular calcium concentration in H9c2 cardiomyoctes. In addition, baicalein also inhibited lysoPC-induced apoptosis, with associated decreased pro-apoptotic Bax protein, increased anti-apoptotic Bcl-2 protein, resulting in an increase in the Bcl-2/Bax ratio. Finally, baicalein attenuated lysoPC-induced the expression of cytochrome c, casapase-3, casapase-9, and the phosphorylations of ERK1/2, JNK, and p38. LysoPC-induced ERK1/2, JNK, and p38 activations were inhibited by baicalein. CONCLUSIONS: Baicalein protects cardiomyocytes from lysoPC-induced apoptosis by reducing ROS production, inhibition of calcium overload, and deactivations of MAPK signaling pathways. SN - 1472-6882 UR - https://www.unboundmedicine.com/medline/citation/25012390/Baicalein_an_active_component_of_Scutellaria_baicalensis_Georgi_prevents_lysophosphatidylcholine_induced_cardiac_injury_by_reducing_reactive_oxygen_species_production_calcium_overload_and_apoptosis_via_MAPK_pathways_ L2 - https://bmccomplementalternmed.biomedcentral.com/articles/10.1186/1472-6882-14-233 DB - PRIME DP - Unbound Medicine ER -