Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H2O2-Induced Cell Apoptosis through Akt Signalling

被引:25
作者
Lee, Mu-Jang [1 ]
Chen, Han-Min [2 ]
Tzang, Bor-Show [3 ]
Lin, Chiu-Wen [3 ]
Wang, Chau-Jong [3 ]
Liu, Jer-Yuh [4 ,5 ]
Kao, Shao-Hsuan [3 ,6 ]
机构
[1] Tian Sheng Mem Hosp, Div Cardiol, Dept Internal Med, Pingtung 92843, Taiwan
[2] Fu Jen Catholic Univ, Dept Life Sci, Taipei 24205, Taiwan
[3] Chung Shan Med Univ, Inst Biochem & Biotechnol, Taichung 40201, Taiwan
[4] China Med Univ, Grad Inst Canc Biol, Taichung 40402, Taiwan
[5] China Med Univ Hosp, Ctr Mol Med, Taichung 40402, Taiwan
[6] Chung Shan Med Univ Hosp, Clin Lab, Taichung 40201, Taiwan
关键词
NF-KAPPA-B; CYTOCHROME-C; IN-VITRO; ACTIVATION; DEATH; ANTIOXIDANTS; KINASES; GROWTH; MITOCHONDRIA; RADICALS;
D O I
10.1155/2011/578060
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Increased cell death of cardiomyocyte by oxidative stress is known to cause dysfunction of the heart. O. gratissimum is one of the more well-known medicinal plants among the Ocimum species and widely used in treatment of inflammatory diseases. In this study, we hypothesized that aqueous extract of O. gratissimum leaf (OGE) may protect myocardiac cell H9c2 from oxidative injury by hydrogen peroxide (H2O2). Our results revealed that OGE pretreatment dose-dependently protects H9c2 cells from cell death when exposed to H2O2. Additionally, DNA condensation induced by H2O2 was also reduced by OGE pretreatment, suggesting that Ocimum gratissimum extract may attenuate H2O2-induced chromosome damage. Further investigation showed that OGE pretreatment inhibited H2O2-induced activation of caspase-3 and caspase-9, as well as H2O2-induced upregulation of proapoptotic Apaf-1 and the release of cytosolic cytochrome c, but has little effect on the activation of caspase-8. Additionally, OGE pretreatment significantly upregulated Bcl-2 expression and Akt phosphorylation, and slightly affected the phosphorylation of mitogen-activated protein kinases including p38MAPK and JNK. Taken together, our findings revealed that Ocimum gratissimum extract effectively inhibited the mitochondrial pathway and upregulated Bcl-2 expression, which may be important in protecting H9c2 cells from H2O2-induced cell death.
引用
收藏
页数:8
相关论文
共 48 条
  • [1] Hypoglycaemic activity of Ocimum gratissimum in rats
    Aguiyi, JC
    Obi, CI
    Gang, SS
    Igweh, AC
    [J]. FITOTERAPIA, 2000, 71 (04) : 444 - 446
  • [2] The survival kinases Akt and Pim as potential pharmacological targets
    Amaravadi, R
    Thompson, CB
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (10) : 2618 - 2624
  • [3] Role of quercetin and its in vivo metabolites in protecting H9c2 cells against oxidative stress
    Angeloni, C.
    Spencer, J. P. E.
    Leoncini, E.
    Biagi, P. L.
    Hrelia, S.
    [J]. BIOCHIMIE, 2007, 89 (01) : 73 - 82
  • [4] IMMUNOMODULATING AGENTS OF PLANT-ORIGIN .1. PRELIMINARY SCREENING
    ATAL, CK
    SHARMA, ML
    KAUL, A
    KHAJURIA, A
    [J]. JOURNAL OF ETHNOPHARMACOLOGY, 1986, 18 (02) : 133 - 141
  • [5] Comparative in vitro effects of AZT and extracts of Ocimum gratissimum, Ficus polita, Clausena anisata, Alchornea cordifolia, and Elaeophorbia drupifera against HIV-1 and HIV-2 infections
    Ayisi, NK
    Nyadedzor, C
    [J]. ANTIVIRAL RESEARCH, 2003, 58 (01) : 25 - 33
  • [6] Aziba PI, 1999, PHYTOTHER RES, V13, P427, DOI 10.1002/(SICI)1099-1573(199908/09)13:5<427::AID-PTR467>3.0.CO
  • [7] 2-T
  • [8] Bishopric Nanette H., 2001, Current Opinion in Pharmacology, V1, P141, DOI 10.1016/S1471-4892(01)00032-7
  • [9] Regulation of cell death protease caspase-9 by phosphorylation
    Cardone, MH
    Roy, N
    Stennicke, HR
    Salvesen, GS
    Franke, TF
    Stanbridge, E
    Frisch, S
    Reed, JC
    [J]. SCIENCE, 1998, 282 (5392) : 1318 - 1321
  • [10] Hibiscus sabdariffa extract inhibits the development of atherosclerosis in cholesterol-fed rabbits
    Chen, CC
    Hsu, JD
    Wang, SF
    Chiang, HC
    Yang, MY
    Kao, ES
    Ho, YC
    Wang, CJ
    [J]. JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY, 2003, 51 (18) : 5472 - 5477