title: Improvement of radiation-induced healing delay by etanercept treatment in rat arteries.
abstract: Surgical treatment often causes difficulty in the irradiated field because of delayed wound healing, which is mainly due to vascular dysfunction. To overcome this difficulty, we attempted to accelerate the recovery from clamp injury in irradiated superficial epigastric arteries of rats as a model. Etanercept, a soluble receptor of tumor necrosis factor-alpha, was administered four times to rats with irradiated arteries before and after clamp injury. Loss of endothelial cells and necrosis of the media in the irradiated arteries continued for more than 1 week after the injury; however, in the rats treated with etanercept, the endothelial cells recovered in the intima, and alpha-smooth muscle actin-positive smooth muscle cells recovered in the injured and irradiated arteries. After clamp injury of common carotid arteries that had previously been irradiated, the blood flow in these arteries was visualized by magnetic resonance (MR) angiography. The time-of-flight signal was weakened in the injured and irradiated arteries. This time-of-flight signal was recovered by the etanercept treatment. These findings suggest that etanercept improves the radiation-impaired healing of arteries in rats.
authors.affiliation: Experimental Animal Laboratory, Kashiwa, Chiba 277-8577, Japan. ksugiyam@east.ncc.go.jp
authors.forename: Kenji
authors.initials: K
authors.lastname: Sugiyama
authors.forename: Masayuki
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Junichiro
authors.initials: J
authors.lastname: Kuroda
authors.forename: Masakazu
authors.initials: M
authors.lastname: Takanashi
authors.forename: Yukio
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Fujii
authors.forename: Toshiharu
authors.initials: T
authors.lastname: Ishii
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Esumi
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D001158:Arteries / Q000293:injuries* / Q000473:pathology; D020212:Carotid Artery Injuries / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000473:pathology; D019074:Epigastric Arteries / Q000293:injuries / Q000473:pathology; D000068800:Etanercept; D005260:Female; D007074:Immunoglobulin G / Q000627:therapeutic use*; D018810:Magnetic Resonance Angiography; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000503:physiopathology; D009336:Necrosis / Q000473:pathology; D011827:Radiation; D051381:Rats; D011916:Rats, Inbred F344; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012039:Regional Blood Flow; D012995:Solubility; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology; D014945:Wound Healing
chemical_list: D000199:Actins; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000068800:Etanercept