Metabolites of scutellariae radix inhibit injury of endothelial cells in hypoxia device

Chia Lun Chao, Shiuan Pey Lin, Yu Chi Hou, Pei Dawn Lee Chao, Nen Chung Chang, Yu Ching Huang, Feng Ming Ho

Research output: Contribution to journalArticlepeer-review


The effects of the metabolites of Scutellariae Radix (SR), a traditional anti-inflammatory oriental herbal medicine, on hypoxia/reoxygenation (H/R)-induced inflammation and apoptosis of human umbilical vein endothelial cells (HUVECs) were investigated. SR metabolites (SRMs) were prepared from the sulfatase/β-glucuronidase-added serum of SR-decoction-fed rats and examined using highperformance liquid chromatography. HUVECs were put into a mechanical device conditioned with hypoxia (94 %N2, 5 % CO2, and 1 %O2) for 4 h (H4), and then reoxygenation (room air with 5 % CO2) for 4 h (R4), alone or in the presence of SRMs or vitamin C. Cell adhesion and apoptosis were detected using the enzyme-linked immunosorbent assay. Intercellular adhesion molecule-1 (ICAM-1), cyclooxygenase-2 (COX-2), caspase-3, and heme oxygenase-1 (HO-1) were evaluated using western blotting. COX-2 small hairpin RNA (shRNA) and HO-1 shRNA were used to evaluate the relationship of COX-2 and HO-1 to cell apoptosis. THP-1 adhesion, and ICAM-1 and COX-2 expression increased at H4 and H4/R4, but decreased at H8, and could be ameliorated by SRMs in a dose-dependent manner. Notedly, SRMs effectively attenuated COX-2-mediated cell apoptosis, which was enhanced byHO-1 shRNA, especially atH4/R4 injury. In conclusion, in a hypoxia chamber that mimics the hypoxic condition in acute coronary syndrome, SRMs protected H/Rinduced inflammation and the death of endothelial cells via oxidative stress reduction.

Original languageEnglish
Pages (from-to)492-499
Number of pages8
JournalJournal of Medical and Biological Engineering
Issue number4
Publication statusPublished - Aug 2015


  • Apoptosis
  • Cyclooxygenase-2
  • Endothelial cells
  • Hypoxia
  • Inflammation
  • Scutellariae radix

ASJC Scopus subject areas

  • Biomedical Engineering


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