ABSTRACT
OBJECTIVE: To evaluate the effects of hyperbaric oxygen (HBO) therapy in the management of chronic wound and observe the correlation between wound healing and CD34+ endothelial progenitor cells (EPCs). METHODS: A total of 119 patients with chronic wound in lower extremities lasting > 3 months were recruited for this randomized, single-center, placebo-controlled clinical trial. The changes of CD34+ average count before and after HBO therapy were detected by flow cytometry (FACS). There were 97 patients on long-term HBO therapy and in 22 patients on hyperbaric air therapy as control group. The CD34/Scal-1+ and CD34/CXCR4 dual-positive populations of gated cell were determined respectively by FACs. The outcomes of two groups were compared. Treatment was administered within a single-place hyperbaric chamber for 90-min daily (session duration 120 min) for 5 days a week for 4 weeks (20 treatment sessions). RESULTS: The wound size decreased at the 4-week end point (62.7% ± 22.3% in the HBO group vs 34.4% ± 20.6% in the control group, P < 0.05). After 10 episodes of HBO therapies for chronic non-healing wound, the peripheral CD34+ EPCs average count rose from 0.24% ± 0.03% at pre-treatment to 1.32% ± 0.05% while the number was 1.75% ± 0.17% after 20 episodes of HBO (P < 0.05). Both were significantly different from that of the patients at pre-treatment. However the overall circulating white cell count was not significantly elevated. The CD34/Scal-1+ and CD34/CXCR4 dual-positive populations of gated cell in HBO group were 5.8 and 5.2 folds than those at pre-treatment respectively. The number of EPCs was positively correlated with wound healing in lower extremities (correlation coefficient 0.84; P < 0.01). CONCLUSION: Adjunctive treatment of HBO facilitates the healing of chronic non-healing wound in selected patients through the mobilization of EPCs.
Subject(s)
Hyperbaric Oxygenation , Wound Healing , Wounds and Injuries/blood , Wounds and Injuries/therapy , Adult , Antigens, CD34 , Endothelial Cells/physiology , Female , Humans , Lower Extremity , Male , Middle Aged , Stem Cells/physiologyABSTRACT
OBJECTIVE: To investigate the underlying mechanism of apoptosis-inducing effect of a specific COX-2 inhibitor SC236 in gastric cancer cells. METHODS: Western blot analysis was used to measure apoptosis-related proteins, cytochrome c, and caspase-3. The catalytic activity of the caspases was measured using a colorimetric assay. RESULTS: Treatment of AGS gastric cancer cells with SC236 caused a significant elevation of the pro-apoptotic protein Bak, release of cytochrome c to the cytosol, and activation of caspase-3. A specific caspase-3 inhibitor, z-DEVD-fmk, blocked SC236-induced apoptosis. CONCLUSION: SC236 inhibits cell growth and induces apoptosis in gastric cancer cells at least partly through the up-regulation of Bak, stimulation of cytochrome c release, and activation of caspase-3.
