Thermal treatment attenuates neointimal thickening with enhanced expression of heat-shock protein 72 and suppression of oxidative stress.
BACKGROUND
The beneficial effects of thermal therapy have been reported in several cardiovascular diseases. However, it is unknown whether the thermal treatment has some beneficial roles against the development of atherosclerosis.


RESULTS
The inflammatory arterial lesion was introduced by placement of a polyethylene cuff on femoral arteries of male Sprague-Dawley rats for 4 weeks. Thermal-treated group underwent daily bathing in 41 degrees C hot water for 15 minutes. Neointimal thickening along with immunohistochemical expression of heat-shock proteins (HSPs), monocyte chemoattractant protein-1 (MCP-1), and NADPH oxidase were compared with those of a thermally untreated (Control) group. Morphometric analysis demonstrated a significant suppression of neointimal thickening in thermal-treated group compared with the Control group (intimal/medial area ratios, 0.01+/-0.01 versus 0.31+/-0.04, P<0.01). Expression of MCP-1 and infiltration of ED-positive cells were enhanced in the adventitial layer of Control. More importantly, expression of HSP72 in media was enhanced by thermal treatment. Expression of p22-phox, the major membrane subunit of NADPH oxidase, and MCP-1 was augmented in cuff-injured adventitia of the Control but not the thermal-treated groups.


CONCLUSIONS
Thermal treatment significantly attenuated infiltration of inflammatory cells in adventitia and suppressed neointimal thickening in cuff-injured arteries with the enhancement of HSP72 expression and suppression of oxidative stress.
Okada
Motoi
M
First Department of Medicine, Asahikawa Medical College, Asahikawa, Japan.
Hasebe
Naoyuki
N
Aizawa
Yoshiaki
Y
Izawa
Kazuma
K
Kawabe
Jun-ichi
J
Kikuchi
Kenjiro
K
D000818:Animals; D001013:Aorta, Thoracic; D001161:Arteriosclerosis / Q000473:pathology / Q000517:prevention & control*; D001494:Baths; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D004195:Disease Models, Animal; D005263:Femoral Artery / Q000293:injuries / Q000473:pathology*; D005347:Fibroblasts / Q000378:metabolism; D005786:Gene Expression Regulation; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D006358:Hot Temperature; D006979:Hyperthermia, Induced; D006984:Hypertrophy; D020007:Implants, Experimental / Q000009:adverse effects; D008297:Male; D026901:Membrane Transport Proteins / Q000096:biosynthesis / Q000235:genetics; D009252:NADPH Dehydrogenase / Q000096:biosynthesis / Q000235:genetics; D019255:NADPH Oxidases; D018384:Oxidative Stress; D010750:Phosphoproteins / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species; D017539:Tunica Intima / Q000648:ultrastructure*; D014657:Vasculitis / Q000473:pathology / Q000517:prevention & control
C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D026901:Membrane Transport Proteins; D010750:Phosphoproteins; D017382:Reactive Oxygen Species; D019255:NADPH Oxidases; C086986:CYBA protein, human; D009252:NADPH Dehydrogenase