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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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Effects of IFR radiation on eNOS, Akt, p-ERK, p-38 MAPK, VEGF and HO-1 production in cultured EPCs. Administration of IFR radiation on cultured ECFCs for 10, 30, and 40 min followed by treatment of EPCs in high-glucose conditions significantly upregulated high glucose-impaired eNOS production and eNOS activity (p-eNOS/total eNOS). Treatment of IFR therapy for 30, 40 and 60 min also upregulated Akt activation (p-Akt/total Akt). In addition, administration IFR radiation also promoted VEGF production, p-ERK, and p-38 MAPK in high glucose conditions, but not HO-1. Each bar graph shows the summarized data from four separate experiments by densitometry after normalization. Data are means ± SEM; n = 4 in each experiment. (*p < 0.05 compared with control; #p < 0.05 compared with HG group.).
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Figure 5: Effects of IFR radiation on eNOS, Akt, p-ERK, p-38 MAPK, VEGF and HO-1 production in cultured EPCs. Administration of IFR radiation on cultured ECFCs for 10, 30, and 40 min followed by treatment of EPCs in high-glucose conditions significantly upregulated high glucose-impaired eNOS production and eNOS activity (p-eNOS/total eNOS). Treatment of IFR therapy for 30, 40 and 60 min also upregulated Akt activation (p-Akt/total Akt). In addition, administration IFR radiation also promoted VEGF production, p-ERK, and p-38 MAPK in high glucose conditions, but not HO-1. Each bar graph shows the summarized data from four separate experiments by densitometry after normalization. Data are means ± SEM; n = 4 in each experiment. (*p < 0.05 compared with control; #p < 0.05 compared with HG group.).

Mentions: We investigated the effects of IFR radiation on high glucose-treated EPCs to determine whether IFR therapy could recover impaired eNOS activation in EPCs. Administration of IFR radiation on cultured ECFCs for 10, 30, and 40 min followed by treatment of EPCs in high glucose conditions significantly upregulated high glucose-impaired eNOS production and eNOS activity (p-eNOS/total eNOS). Treatment of IFR therapy for 30, 40 and 60 min also upregulated Akt activation (p-Akt/total Akt). In addition, administration IFR radiation also promoted VEGF production, p-ERK, and p-38 MAPK in high glucose conditions, but not HO-1 (Figure 5). These findings suggested that treatment with IFR radiation may enhance activities of eNOS, Akt, p-ERK, p-38 MAPK and VEGF production in EPCs in response to high glucose stimulation.


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)

Effects of IFR radiation on eNOS, Akt, p-ERK, p-38 MAPK, VEGF and HO-1 production in cultured EPCs. Administration of IFR radiation on cultured ECFCs for 10, 30, and 40 min followed by treatment of EPCs in high-glucose conditions significantly upregulated high glucose-impaired eNOS production and eNOS activity (p-eNOS/total eNOS). Treatment of IFR therapy for 30, 40 and 60 min also upregulated Akt activation (p-Akt/total Akt). In addition, administration IFR radiation also promoted VEGF production, p-ERK, and p-38 MAPK in high glucose conditions, but not HO-1. Each bar graph shows the summarized data from four separate experiments by densitometry after normalization. Data are means ± SEM; n = 4 in each experiment. (*p < 0.05 compared with control; #p < 0.05 compared with HG group.).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Effects of IFR radiation on eNOS, Akt, p-ERK, p-38 MAPK, VEGF and HO-1 production in cultured EPCs. Administration of IFR radiation on cultured ECFCs for 10, 30, and 40 min followed by treatment of EPCs in high-glucose conditions significantly upregulated high glucose-impaired eNOS production and eNOS activity (p-eNOS/total eNOS). Treatment of IFR therapy for 30, 40 and 60 min also upregulated Akt activation (p-Akt/total Akt). In addition, administration IFR radiation also promoted VEGF production, p-ERK, and p-38 MAPK in high glucose conditions, but not HO-1. Each bar graph shows the summarized data from four separate experiments by densitometry after normalization. Data are means ± SEM; n = 4 in each experiment. (*p < 0.05 compared with control; #p < 0.05 compared with HG group.).
Mentions: We investigated the effects of IFR radiation on high glucose-treated EPCs to determine whether IFR therapy could recover impaired eNOS activation in EPCs. Administration of IFR radiation on cultured ECFCs for 10, 30, and 40 min followed by treatment of EPCs in high glucose conditions significantly upregulated high glucose-impaired eNOS production and eNOS activity (p-eNOS/total eNOS). Treatment of IFR therapy for 30, 40 and 60 min also upregulated Akt activation (p-Akt/total Akt). In addition, administration IFR radiation also promoted VEGF production, p-ERK, and p-38 MAPK in high glucose conditions, but not HO-1 (Figure 5). These findings suggested that treatment with IFR radiation may enhance activities of eNOS, Akt, p-ERK, p-38 MAPK and VEGF production in EPCs in response to high glucose stimulation.

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