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Far infra-red therapy promotes ischemia-induced angiogenesis in diabetic mice and restores high glucose-suppressed endothelial progenitor cell functions.

Huang PH, Chen JW, Lin CP, Chen YH, Wang CH, Leu HB, Lin SJ - Cardiovasc Diabetol (2012)

Bottom Line: Far infra-red (IFR) therapy was shown to exert beneficial effects in cardiovascular system, but effects of IFR on endothelial progenitor cell (EPC) and EPC-related vasculogenesis remain unclear.Doppler perfusion imaging demonstrated that the ischemic limb/normal side blood perfusion ratio in the thermal therapy group was significantly increased beyond that in controls, and significantly greater capillary density was seen in the IFR therapy group.In in-vitro studies, cultured EPCs treated with IFR radiation markedly augmented high glucose-impaired EPC functions, inhibited high glucose-induced EPC senescence and reduced H(2)O(2) production.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Cardiology, Taipei Veterans General Hospital, Taipei, Taiwan.

ABSTRACT

Background: Far infra-red (IFR) therapy was shown to exert beneficial effects in cardiovascular system, but effects of IFR on endothelial progenitor cell (EPC) and EPC-related vasculogenesis remain unclear. We hypothesized that IFR radiation can restore blood flow recovery in ischemic hindlimb in diabetic mice by enhancement of EPCs functions and homing process.

Materials and methods: Starting at 4 weeks after the onset of diabetes, unilateral hindlimb ischemia was induced in streptozotocin (STZ)-induced diabetic mice, which were divided into control and IFR therapy groups (n = 6 per group). The latter mice were placed in an IFR dry sauna at 34°C for 30 min once per day for 5 weeks.

Results: Doppler perfusion imaging demonstrated that the ischemic limb/normal side blood perfusion ratio in the thermal therapy group was significantly increased beyond that in controls, and significantly greater capillary density was seen in the IFR therapy group. Flow cytometry analysis showed impaired EPCs (Sca-1(+)/Flk-1(+)) mobilization after ischemia surgery in diabetic mice with or without IFR therapy (n = 6 per group). However, as compared to those in the control group, bone marrow-derived EPCs differentiated into endothelial cells defined as GFP(+)/CD31(+) double-positive cells were significantly increased in ischemic tissue around the vessels in diabetic mice that received IFR radiation. In in-vitro studies, cultured EPCs treated with IFR radiation markedly augmented high glucose-impaired EPC functions, inhibited high glucose-induced EPC senescence and reduced H(2)O(2) production. Nude mice received human EPCs treated with IFR in high glucose medium showed a significant improvement in blood flow recovery in ischemic limb compared to those without IFR therapy. IFR therapy promoted blood flow recovery and new vessel formation in STZ-induced diabetic mice.

Conclusions: Administration of IFR therapy promoted collateral flow recovery and new vessel formation in STZ-induced diabetic mice, and these beneficial effects may derive from enhancement of EPC functions and homing process.

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IFR therapy decreased reactive oxidative stress, recovered EPC proliferation, and increased NO production in high-glucose conditions. (A) High glucose markedly increased H2O2 production determined by the relative DCFH-DA fluorescent intensity, and the administration of IFR therapy suppressed high glucose-induced reactive oxidative stress (ROS) index in EPCs culture. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min) (B) The effect of IFR radiation on EPCs proliferation was analyzed by MTT assay. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min) (C) Nitrate production (as NO content) in culture medium was measured by Griess reagent. High glucose-suppressed NO production in cultured late EPC s. After 4 days of incubation, IFR radiation increased NO production with or with high glucose conditions. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min; **p < 0.05 compared with control – 0 min; n = 4 for each experiment).
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Figure 4: IFR therapy decreased reactive oxidative stress, recovered EPC proliferation, and increased NO production in high-glucose conditions. (A) High glucose markedly increased H2O2 production determined by the relative DCFH-DA fluorescent intensity, and the administration of IFR therapy suppressed high glucose-induced reactive oxidative stress (ROS) index in EPCs culture. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min) (B) The effect of IFR radiation on EPCs proliferation was analyzed by MTT assay. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min) (C) Nitrate production (as NO content) in culture medium was measured by Griess reagent. High glucose-suppressed NO production in cultured late EPC s. After 4 days of incubation, IFR radiation increased NO production with or with high glucose conditions. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min; **p < 0.05 compared with control – 0 min; n = 4 for each experiment).

Mentions: High glucose markedly increased H2O2 production determined by the relative DCFH-DA fluorescent intensity, and administration of IFR radiation (10–60 mins) significantly suppressed the high glucose-induced ROS index in cultures of ECFCs (Figure 4A).


Far infra-red therapy promotes ischemia-induced angiogenesis in diabetic mice and restores high glucose-suppressed endothelial progenitor cell functions.

Huang PH, Chen JW, Lin CP, Chen YH, Wang CH, Leu HB, Lin SJ - Cardiovasc Diabetol (2012)

IFR therapy decreased reactive oxidative stress, recovered EPC proliferation, and increased NO production in high-glucose conditions. (A) High glucose markedly increased H2O2 production determined by the relative DCFH-DA fluorescent intensity, and the administration of IFR therapy suppressed high glucose-induced reactive oxidative stress (ROS) index in EPCs culture. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min) (B) The effect of IFR radiation on EPCs proliferation was analyzed by MTT assay. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min) (C) Nitrate production (as NO content) in culture medium was measured by Griess reagent. High glucose-suppressed NO production in cultured late EPC s. After 4 days of incubation, IFR radiation increased NO production with or with high glucose conditions. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min; **p < 0.05 compared with control – 0 min; n = 4 for each experiment).
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC3472269&req=5

Figure 4: IFR therapy decreased reactive oxidative stress, recovered EPC proliferation, and increased NO production in high-glucose conditions. (A) High glucose markedly increased H2O2 production determined by the relative DCFH-DA fluorescent intensity, and the administration of IFR therapy suppressed high glucose-induced reactive oxidative stress (ROS) index in EPCs culture. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min) (B) The effect of IFR radiation on EPCs proliferation was analyzed by MTT assay. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min) (C) Nitrate production (as NO content) in culture medium was measured by Griess reagent. High glucose-suppressed NO production in cultured late EPC s. After 4 days of incubation, IFR radiation increased NO production with or with high glucose conditions. (*p < 0.05 compared with control - 0 min; #p < 0.05 compared with high glucose - 0 min; **p < 0.05 compared with control – 0 min; n = 4 for each experiment).
Mentions: High glucose markedly increased H2O2 production determined by the relative DCFH-DA fluorescent intensity, and administration of IFR radiation (10–60 mins) significantly suppressed the high glucose-induced ROS index in cultures of ECFCs (Figure 4A).

Bottom Line: Far infra-red (IFR) therapy was shown to exert beneficial effects in cardiovascular system, but effects of IFR on endothelial progenitor cell (EPC) and EPC-related vasculogenesis remain unclear.Doppler perfusion imaging demonstrated that the ischemic limb/normal side blood perfusion ratio in the thermal therapy group was significantly increased beyond that in controls, and significantly greater capillary density was seen in the IFR therapy group.In in-vitro studies, cultured EPCs treated with IFR radiation markedly augmented high glucose-impaired EPC functions, inhibited high glucose-induced EPC senescence and reduced H(2)O(2) production.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Cardiology, Taipei Veterans General Hospital, Taipei, Taiwan.

ABSTRACT

Background: Far infra-red (IFR) therapy was shown to exert beneficial effects in cardiovascular system, but effects of IFR on endothelial progenitor cell (EPC) and EPC-related vasculogenesis remain unclear. We hypothesized that IFR radiation can restore blood flow recovery in ischemic hindlimb in diabetic mice by enhancement of EPCs functions and homing process.

Materials and methods: Starting at 4 weeks after the onset of diabetes, unilateral hindlimb ischemia was induced in streptozotocin (STZ)-induced diabetic mice, which were divided into control and IFR therapy groups (n = 6 per group). The latter mice were placed in an IFR dry sauna at 34°C for 30 min once per day for 5 weeks.

Results: Doppler perfusion imaging demonstrated that the ischemic limb/normal side blood perfusion ratio in the thermal therapy group was significantly increased beyond that in controls, and significantly greater capillary density was seen in the IFR therapy group. Flow cytometry analysis showed impaired EPCs (Sca-1(+)/Flk-1(+)) mobilization after ischemia surgery in diabetic mice with or without IFR therapy (n = 6 per group). However, as compared to those in the control group, bone marrow-derived EPCs differentiated into endothelial cells defined as GFP(+)/CD31(+) double-positive cells were significantly increased in ischemic tissue around the vessels in diabetic mice that received IFR radiation. In in-vitro studies, cultured EPCs treated with IFR radiation markedly augmented high glucose-impaired EPC functions, inhibited high glucose-induced EPC senescence and reduced H(2)O(2) production. Nude mice received human EPCs treated with IFR in high glucose medium showed a significant improvement in blood flow recovery in ischemic limb compared to those without IFR therapy. IFR therapy promoted blood flow recovery and new vessel formation in STZ-induced diabetic mice.

Conclusions: Administration of IFR therapy promoted collateral flow recovery and new vessel formation in STZ-induced diabetic mice, and these beneficial effects may derive from enhancement of EPC functions and homing process.

Show MeSH
Related in: MedlinePlus