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07-08-2026

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REGULATORY POTENTIAL OF RHIZOME EXTRACT FROM PARIS POLYPHYLLA VAR. YUNANENSIS ON PRO-APOPTOTIC PROTEINS IN A549 LUNG CANCER CELLS. (2026). Tạp Chí Dược liệu, 3(28), pp. 191 - 196. https://doi.org/10.63240/jmm-nimm.2023.28.356

REGULATORY POTENTIAL OF RHIZOME EXTRACT FROM PARIS POLYPHYLLA VAR. YUNANENSIS ON PRO-APOPTOTIC PROTEINS IN A549 LUNG CANCER CELLS

Các tác giả

    Ly Hai Trieu 1 # , Le Thi Kim Oanh 1 , Le Van Minh 1
  • 1 Research Center of Ginseng and Medicinal Materials, National Institute of Medicinal Materials, Ho Chi Minh City, Vietnam

DOI:

https://doi.org/10.63240/jmm-nimm.2023.28.356

Từ khóa:

Paris polyphylla var. yunanensis, Rhizome extract, Apoptosis, Cytotoxicity, A549

Tóm tắt

Paris polyphylla var. yunanensis has been shown to affect against various types of cancer cells. The aim of this study was to investigate the effects of 80% ethanol extract from Paris polyphylla var. yunanensis rhizomes (PPRE) on cell proliferation and apoptosis in a non-small cell lung cancer cell line (A549) in vitro via expression of apoptosis-related proteins using western blot. Our result showed that PPRE at 2.5, 5, and 10 μg/mL concentrations significantly inhibited A549 cell proliferation in a dose-dependent manner after 24 and 48 h of treatment. Furthermore, A549 cells were treated with the PPRE at the concentrations of 4.5, 5.0, and 5.5 μg/mL for 24 h showed markedly higher Bcl-2-associated X (Bax) protein expression levels, significantly lower Bcl-2 expression levels, and obviously notably higher Bax/Bcl-2 ratio than the control. Meanwhile, the p53 protein expression levels were not significantly reduced compared to the control by the PPRE. The findings of this study implicate that Paris polyphylla var. yunanensis rhizome extract may be a potential candidate to inhibit the proliferation of A549 cells and promote apoptosis by the Bcl-2/Bax pathways. Studying the effect of PPRE on some other molecular markers involved in programmed cell death should be done to elucidate the mechanism of A549 human lung cancer cell apoptosis of the PPRE.

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