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Oridonin induces G2/M cell cycle arrest and apoptosis through MAPK and p53 signaling pathways in HepG2 cells

Hui Wang1, Yan Ye, Jian-Hong Chui

  • 1Center for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong, PR China.

Oncology Reports
|July 29, 2010
PubMed

Insights

Oridonin, derived from Isodon rubescen, effectively reduces liver cancer cell viability. It triggers G2/M cell cycle arrest and apoptosis via MAPK and p53 pathways, offering new insights into hepatocarcinoma management.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Hepatocellular Carcinoma Research

Background:

  • Oridonin is the primary active compound in Isodon rubescen.
  • It exhibits known antihepatocarcinoma activity in preclinical and clinical studies.

Purpose of the Study:

  • To investigate the anticancer effects of oridonin on HepG2 liver cancer cells.
  • To elucidate the molecular mechanisms underlying oridonin's action.

Main Methods:

  • Cell viability assays (MTT) to determine IC50 values.
  • Flow cytometry for cell cycle analysis and apoptosis detection.
  • DAPI staining for nuclear morphology.
  • Western blotting to assess protein expression (MAPK pathway, p53, caspases).

Main Results:

  • Oridonin dose- and time-dependently decreased HepG2 cell viability (IC50: 38.86 µM at 24h, 24.90 µM at 48h).
  • Induced G2/M cell cycle arrest and apoptosis, evidenced by nuclear changes.
  • Modulated MAPK signaling (increased p-JNK, p-p38, p-p53, p21; decreased p-ERK) and activated caspase-3 and caspase-9.

Conclusions:

  • Oridonin effectively induces G2/M cell cycle arrest and apoptosis in HepG2 cells.
  • The mechanisms involve the activation of MAPK and p53 signaling pathways.
  • Findings contribute to understanding oridonin's role in managing hepatocarcinoma.

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