4.4 Article

Paeonol triggers apoptosis in HeLa cervical cancer cells: the role of mitochondria-related caspase pathway

Journal

PSYCHOPHARMACOLOGY
Volume 239, Issue 7, Pages 2083-2092

Publisher

SPRINGER
DOI: 10.1007/s00213-021-05811-0

Keywords

Paeonol; HeLa cells; Apoptosis; Mitochondrial pathway

Funding

  1. Guangdong Natural Science Foundation [2018A030313084]
  2. Administration of Traditional Chinese Medicine of Guangdong Province of China [20191187]
  3. Public Service Platform Open Project Fund of South China Sea for R&D Marine Biomedicine Resources [2HC18010]
  4. Educational Commission of Guangdong Province [4SG20124G, 4SG20126G]
  5. Guangdong Medical University [GDMUZ2020005]

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Paeonol demonstrates anti-cervical cancer potential by inhibiting proliferation, inducing apoptosis, and triggering cellular apoptosis through the mitochondrial pathway, which involves downregulating PI3K/Akt signaling.
Paeonol is a biologically active component purified from the root bark of Cortex Moutan that exerts pharmacological effects on the cervical cancer. In this study, we aim to evaluate the anti-cervical cancer capacity of paeonol and to investigate the mechanism driving its anti-cervical cancer effect. Paeonol administration markedly restrained the proliferation and caused apoptosis in HeLa cells. Furthermore, paeonol treatment resulted in a mitochondrial dysfunction in HeLa cells, including the inducing of mitochondrial membrane potential (MMP), reactive oxygen species (ROS) production, and the release of cytochrome c. Moreover, the Bcl-2/Bax proportion was obviously downregulated and cleaved caspase-3 expression was evaluated through paeonol treatment. Additionally, the expression of p-PI3K and p-Akt was noticeably reduced in response to paeonol treatment in HeLa cells. Our findings indicated that paeonol exerts an anticancer potential in HeLa cells, at least in a manner, via triggering the mitochondrial pathway of cellular apoptosis by inhibiting PI3K/Akt signaling. Thus, paeonol has great potential as a promising therapeutic compound to resist human cervical cancer.

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