Abstract for presentation at Australia and New Zealand Society of Nephrology Annual Scientific Conference

Protective effect of Angelica sinensis on renal vascular endothelial cell damage induced by oxidative stress

  • Ms Miko Yamada, Molecular and Cellular Pathology, University of Queensland, Australia
  • Dr David Vesey, Renal Medicine, Princess Alexandra Hospital, Australia
  • Prof David Johnson, Renal Medicine, Princess Alexandra Hospital, Australia
  • A/Prof Glenda Gobe, Molecular and Cellular Pathology, University of Queensland, Australia

    • Purpose: A key factor in the pathogenesis of acute renal failure (ARF) is damage to the vascular endothelium by oxidative stress. Angelica sinensis (AS) alleviates cerebral ischemic damage via anti-oxidant activity. Its use in ARF is not known. We aimed to test endothelial cell protection or regeneration by AS during oxidative stress.
    Methods: Renal medullary and aortic vascular endothelial cells (RMVEC and BAEC) were treated in growth medium with 0.8 or 0.6mM H2O2 (RMVEC or BAEC), or with an approximate pO2 of 50 (hypoxia), with or without AS extract. Controls were not treated. Oxidative stress (hemeoxygenase-1, HO-1), apoptosis, mitosis and activated caspase-3 were analysed at 20hrs.
    Results: Apoptosis and mitosis in controls were, respectively, 0.12+/-0.02% and 0.55+/-0.04% for RMVEC and 0.18+/-0.12% and 1.75+/-0.12% for BAEC. H2O2: increased apoptosis (10.74+/-1.17% in RMVEC and 14.3+/-1.06% in BAEC) (p<0.05) was significantly decreased with AS (4.22+/-0.29% in RMVEC and 3.4+/-0.59% in BAEC) (p<0.05). Activated caspase-3 remained unchanged in RMVEC. A significant increase in caspase-3 expression in H2O2-treated BAEC was decreased with AS (p<0.05). AS stimulated mitosis only in untreated cultures of both cell lines. Hypoxia: only BAECs had decreased mitosis (0.07+/-0.07%) (p<0.05) and increased apoptosis (2.04+/-0.39%) (p<0.05). AS increased mitosis (1.60+/-0.33%) and decreased apoptosis (0.54+/-0.16%) (p<0.05). HO-1 expression was decreased by AS only after hypoxic treatments of BAEC but not after H2O2.
    Conclusion: AS is anti-apoptotic and protects endothelial cells after oxidative stress. Its pro-regenerative action is limited. Its mechanism of action and use in vivo in ARF need further analysis.

    Conference Organiser - ICMS Pty Ltd