Antioxidant therapy attenuates diabetes-related impairment of bone marrow stem cells

Mako Ohshima, Tao Sheng Li, Masayuki Kubo, Shu Lan Qin, Kimikazu Hamano

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)


Background: Bone marrow cells from humans and animals with diabetes exhibit decreased angiogenic potency, thought to be related to oxidative stress, so the present study investigated if antioxidant therapy would attenuate the diabetes-related impairment. Methods and Results: Diabetic mice were given antioxidant therapy, as a daily subcutaneous injection of superoxide dismutase-mimic (10 mg·kg-1·day-1). Diabetic and healthy mice given a vehicle treatment were used as the control. After 4 weeks of treatment, bone marrow mononuclear cells (BM-MNCs) were collected for analysis and the endothelial progenitor cells in BM-MNCs were evaluated by flow cytometry. The intracellular reactive oxygen species (ROS) levels in BM-MNCs were measured using 6-carboxy-2′7′-dichlorodihydrofluorescein diacetate. Endothelial differentiation from the BM-MNCs was estimated by immunostaining with VE-cadherin 7 days after culture. BM-MNCs from the control diabetic mice had fewer Flk-1/CD34 double-positive progenitor cells and higher intracellular ROS levels, with lower potency of endothelial differentiation than BM-MNCs from the healthy mice. Antioxidant therapy decreased the intracellular ROS level in BM-MNCs from that in the diabetic mice significantly (P<0.05), but increased significantly the percentage of endothelial progenitor cells (P<0.05) and their potency of differentiation into endothelial cells (P<0.05). Conclusions: Antioxidant therapy attenuated the diabetes-related impairment of BM-MNCs by reducing oxidative stress.

Original languageEnglish
Pages (from-to)162-166
Number of pages5
JournalCirculation Journal
Issue number1
Publication statusPublished - 2009


  • Angiogenesis
  • Oxidative stress
  • Reactive oxygen species

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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