Trilinolein inhibits proliferation of human non-small cell lung carcinoma A549 through the modulation of PI3K/Akt pathway.
Am J Chin Med
; 39(4): 803-15, 2011.
Article
en En
| MEDLINE
| ID: mdl-21721158
ABSTRACT
Trilinolein has been identified as one of the active constituents isolated from Panax notoginseng used widely in traditional Chinese medicine. Protective actions of Panax notoginseng against cerebral ischemia, beneficial effects on the cardiovascular system, and hemostatic, antioxidant, hypolipidemic, hepatoprotective, renoprotective and estrogen-like activities have been illustrated. In the present study, the effects of trilinolein on the growth of non-small cell lung carcinoma A549 were investigated. It was found that the exposure of A549 cells to trilinolein resulted in the growth inhibition and the induction of apoptosis in a dose- and time- dependent manner. Trilinolein treatment induced the upregulation of pro-apoptotic Bax, downregulation of anti-apoptotic Bcl-2 expression, which was associated with the proteolytic activation of caspases and the concomitant degradation of poly(ADP-ribose) polymerase (PARP) protein. Intracellular reactive oxygen species seem to play a role in the trilinolein-induced apoptosis, since ROS were produced early in the trilinolein treatment. Moreover, the activity of PI3K/Akt was downregulated in trilinolein-treated cells. Our results demonstrated that the most important regulators of trilinolein-induced apoptosis are Bcl-2 family and caspase-3, which are associated with cytochrome c release and dephosphorylation on the Akt signaling pathway.
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Bases de datos:
MEDLINE
Medicinas Tradicionales:
Medicinas_tradicionales_de_asia
/
Medicina_china
Métodos Terapéuticos y Terapias MTCI:
Terapias_biologicas
/
Plantas_medicinales
Asunto principal:
Triglicéridos
/
Carcinoma de Pulmón de Células no Pequeñas
/
Fosfatidilinositol 3-Quinasas
/
Proteínas Proto-Oncogénicas c-akt
/
Panax notoginseng
/
Fitoterapia
/
Antineoplásicos Fitogénicos
Idioma:
En
Revista:
Am J Chin Med
Año:
2011
Tipo del documento:
Article
País de afiliación:
Taiwán