Non-Thermal Effect of Far-Infrared Activates Akt to Reduce Doxorubicin-Induced Apoptosis in Human Umbilical Vein Endothelial Cells

Wen-Sheng Ko ； Tso-Hsiao Chen ； Cheng-Hsien Chen ； Tzen-Wen Chen ； Yen-Cheng Chen

《Acta Nephrologica》 Volume 26 Issue 1 (2012/03) Pp. 2-7

https://doi.org/10.6221/2012.26(1)001

Parallel abstracts

BACKGROUND: The adequacy of hemodialysis is greatly influenced by the long -term patency of vascular access. Far-infrared radiation (FIR) therapy has been proved to be effective in increasing blood flow and inhibiting inflammation of vascular access. However, decreased blood flow may induce apoptosis of endothelial cells. Apoptosis of endothelial cells may stimulate proliferation, migration, and dedifferentiation of vascular smooth muscle cells, thus causing neointimal formation. Ultimately, the vicious cycle of vascular stenosis persists. Our study is to investigate the biological effects of FIR on endothelial cells and elucidate the signaling pathway.METHODS: Human umbilical vein endothelial cells (HUVEC) were pretreated with doxorubicin and then exposed to FIR. The duxoruhicin-induced apoptosis in HUVECs was detected using TUNEL staining. The signals of cleaved caspase-3, caspase-8, caspase-9, and Bcl-2 were detected by Western blotting. The influence of FIR on Akt was analyzed using the phosphoinositide 3-kinase (PI3K) inhibitor. Both thermal and non-thermal effects of FIR were also monitored.RESULTS: FIR exposure for 30 min reduced significantly doxorubicin-induced apoptosis in HUVECs. FIR exposure led to enhancement of phosphorylated-Akt expression in HUVECs. The quantity of cleaved caspase-3, caspase-8 and caspase-9 in doxoruhicin-treated cells al so reduced significantly after FIR exposure. The reduced expression of Bc1-2 was recovered after 30-min FIR exposure. The anti-apoptotic effect of FIR was abolished by Akt inhibitor. In addition, the temperature of culture medium exceeding 37°C attenuated the anti-apoptotic effect of FIR.CONCLUSION: Our data suggest that FIR therapy inhibits the apoptosis of HUVEC via activation of Akt. The nun-thermal effect of anti-apoptosis on endothelial cells may contribute to patency of vascular access.

Parallel keywords

Far-Infrared therapy ； endothelial cell ； apoptosis ； vascular access ； Akt

References

Jones GT, van Rij AM, Packer SG, Walker RJ, Stehbens WE. Venous endothelial changes in therapeutic arteriovenous fistulae. Atherosclerosis 137: 149-156, 1998.

Sho E, Sho M, Singh TM, Xu C, Zarins CK, Masuda H. Blood flow decrease induces apoptosis of endothelial cells in previously dilated arteries resulting from chronic high blood flow. Arterioscler Thromb Vasc Biol 21: 1139-1145, 2001.

Qin F, Dardik H, Pangilinan A, Robinson J, Chuy J, Wengerter K. Remodeling and suppression of intimal hyperplasia of vascular grafts with a distal arteriovenous fistula in a rat model. J Vasc Surg 34: 701-706, 2001.

Kaiser D, Freyberg MA, Friedl P. Lack of hemodynamic forces triggers apoptosis in vascular endothelial cells. Biochem Biophys Res Commun 231: 586-590, 1997.

Berceli SA, Davies MG, Kenagy RD, Clowes AW. Flow-induced neointimal regression in baboon polytetrafluoroethylene grafts is associated with decreased cell proliferation and increased apoptosis. J Vasc Surg 36: 1248-1255, 2002.