PAOD

Ankle brachial index (ABI) is a diagnostic tool for peripheral artery disease (PAD), which is an important issue in hemodialysis (HD) patients. We enrolled 198 maintenance HD patients in this study. PAD is defined as ABI ≤ 0.90. Only PAD patients received far-infrared (FIR) therapy using the WS TY101 FIR emitter for 40 min during each HD session, three times weekly for 6 months. The ABI was measured at the bilateral lower extremities for 4 times [pre-dialytic timing (0 min) and 40 min after the initiation of HD session at both day 0 and 6 months after the FIR therapy]. The primary outcome is the change in ABI. There were 51 out of 198 patients with PAD. In comparison with the period without FIR therapy in the 51 PAD patients, 6 months of FIR therapy significantly improved the ABI of the right/left side for 0 min (from 0.77 ± 0.19 to 0.81 ± 0.20, p = 0.027/0.79 ± 0.20 to 0.81 ± 0.17, p = 0.049), 40 min during HD (from 0.73 ± 0.23 to 0.83 ± 0.19, p < 0.001/from 0.77 ± 0.21 to 0.83 ± 0.18, p < 0.001), and the incremental change between 0 and 40 min (from − 0.04 ± 0.14 to 0.05 ± 0.13, p = 0.007/from − 0.05 ± 0.13 to 0.03 ± 0.11, p = 0.012), respectively. In conclusion, the application of FIR therapy for 40 min, three times weekly for 6 months, has improved the ABI of both lower extremities, thus providing a new strategy of PAD treatment in HD patients.

The accumulation of advanced glycation end products (AGEs) in diabetic patients induces vascular endothelial injury. Promyelocytic leukemia zinc finger protein (PLZF) is a transcription factor that can be activated by low-temperature far-infrared (FIR) irradiation to exert beneficial effects on the vascular endothelium. In the present study, we investigated the influence of FIR-induced PLZF activation on AGE-induced endothelial injury both in vitro and in vivo. FIR irradiation inhibited AGE-induced apoptosis in human umbilical vein endothelial cells (HUVECs). PLZF activation increased the expression of phosphatidylinositol-3 kinases (PI3K), which are important kinases in the autophagic signaling pathway. FIR-induced PLZF activation led to autophagy in HUVEC, which was mediated through the upregulation of PI3K. Immunofluorescence staining showed that AGEs were engulfed by HUVECs and localized to lysosomes. FIR-induced autophagy promoted AGEs degradation in HUVECs. In nicotinamide/streptozotocin-induced diabetic mice, FIR therapy reduced serum AGEs and AGEs deposition at the vascular endothelium. FIR therapy also reduced diabetes-induced inflammatory markers in the vascular endothelium and improved vascular endothelial function. These protective effects of FIR therapy were not found in PLZF-knockout mice. Our data suggest that FIR-induced PLZF activation in vascular endothelial cells protects the vascular endothelium in diabetic mice from AGE-induced injury.

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  Diabetes mellitus (DM) is a metabolic disease that is increasing worldwide. Furthermore, it is associated with the deregulation of vascular-related functions, which can develop into major complications among DM patients. Endothelial colony forming cells (ECFCs) have the potential to bring about medical repairs because of their post-natal angiogenic activities; however, such activities are impaired by high glucose- (HG) and the DM-associated conditions. Far-infrared radiation (FIR) transfers energy as heat that is perceived by the thermoreceptors in human skin. Several studies have revealed that FIR improves vascular endothelial functioning and boost angiogenesis. FIR has been used as anti-inflammatory therapy and as a clinical treatment for peripheral circulation improvement. In addition to vascular repair, there is increasing evidence to show that FIR can be applied to a variety of diseases, including cardiovascular disorders, hypertension and arthritis. Yet mechanism of action of FIR and the biomarkers that indicate FIR effects remain unclear. MicroRNA-134 (miR-134-5p) was identified by small RNA sequencing as being increased in high glucose (HG) treated dfECFCs (HG-dfECFCs). Highly expressed miR-134 was also validated in dmECFCs by RT-qPCR and it is associated with impaired angiogenic activities of ECFCs. The functioning of ECFCs is improved by FIR treatment and this occurs via a reduction in the level of miR-134 and an increase in the NRIP1 transcript, a direct target of miR-134. Using a mouse ischemic hindlimb model, the recovery of impaired blood flow in the presence of HG-dfECFCs was improved by FIR pretreatment and this enhanced functionality was decreased when there was miR-134 overexpression in the FIR pretreated HG-dfECFCs. In conclusion, our results reveal that the deregulation of miR-134 is involved in angiogenic defects found in DM patients. FIR treatment improves the angiogenic activity of HG-dfECFCs and dmECFCs and FIR has potential as a treatment for DM. Detection of miR-134 expression in FIR-treated ECFCs should help us to explore further the effectiveness of FIR therapy.

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    AIMS:

  • Studies have shown that heme oxygenase-1 (HO-1) has a protective role in the mechanism underlying hypoxic preconditioning. We used a far-infrared radiation (FIR) heater to investigate the postconditioning protective role of HO-1against ischemia/reperfusion (I/R) injury in rat testis.

• • MAIN METHODS:
  • Forty rats were used. Testis ischemia was mimicked by total obstructive clamping of testis vessels for 1,2, or 4 h, and concomitant postconditioning with 30 min FIR or heat light during initially 30 min reperfusion. HO-1 expressionand apoptosis of testis tissues were examined by immunohistochemistry and in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay, respectively. HO-1 protein level and caspase-3 activity were analyzed by Western blotting.

• • KEY FINDINGS:
  • There was less apoptotic activity in rat testis after FIR, as determined by TUNEL assay. Higher HO-1 protein expression was observed by immunohistochemistry and Western blotting (p<0.01) in testis cells after FIRpostconditioning. In contrast, caspase-3 activity was significantly higher in heat light groups, as compared with FIR groups (p<0.01).

• SIGNIFICANCE:
• FIR postconditioning attenuated I/R injury in rat testis by inducing HO-1 expression, which might have a protective role in testis apoptosis after I/R injury.