title: Astaxanthin supplementation attenuates immobilization-induced skeletal muscle fibrosis via suppression of oxidative stress.
abstract: Immobilization induces skeletal muscle fibrosis characterized by increasing collagen synthesis in the perimysium and endomysium. Transforming growth factor-β1 (TGF-β1) is associated with this lesion via promoting differentiation of fibroblasts into myofibroblasts. In addition, reactive oxygen species (ROS) are shown to mediate TGF-β1-induced fibrosis in tissues. These reports suggest the importance of ROS reduction for attenuating skeletal muscle fibrosis. Astaxanthin, a powerful antioxidant, has been shown to reduce ROS production in disused muscle. Therefore, we investigated the effects of astaxanthin supplementation on muscle fibrosis under immobilization. In the present study, immobilization increased the collagen fiber area, the expression levels of TGF-β1, α-smooth muscle actin, and superoxide dismutase-1 protein and ROS production. However, these changes induced by immobilization were attenuated by astaxanthin supplementation. These results indicate the effectiveness of astaxanthin supplementation on skeletal muscle fibrosis induced by ankle joint immobilization.
authors.affiliation: Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Suma-ku, Kobe-shi, Hyogo, 654-0142, Japan.
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Maezawa
authors.affiliation: Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Suma-ku, Kobe-shi, Hyogo, 654-0142, Japan.|Department of Physical Therapy, Faculty of Human Sciences, Osaka University of Human Sciences, 1-4-1 Shojaku, Settsu-shi, Osaka, 566-8501, Japan.
authors.forename: Masayuki
authors.initials: M
authors.lastname: Tanaka
authors.affiliation: Department of Physical Therapy, Faculty of Health and Welfare, Prefectural University of Hiroshima, 1-1 Gakuen-cho, Mihara-shi, Hiroshima, 723-0053, Japan.
authors.forename: Miho
authors.initials: M
authors.lastname: Kanazashi
authors.affiliation: Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Suma-ku, Kobe-shi, Hyogo, 654-0142, Japan.
authors.forename: Noriaki
authors.initials: N
authors.lastname: Maeshige
authors.affiliation: Department of Food Science and Nutrition, Nagoya Women's University, Nagoya, 4-21 Shioji-cho, Mizuho-ku, Nagoya-shi, Aichi, 467-8611, Japan.
authors.forename: Hiroyo
authors.initials: H
authors.lastname: Kondo
authors.affiliation: Laboratory of Cell Biology and Life Science, Graduate School of Human and Environmental Studies, Kyoto University, Yoshida-nihonmatsu-cho, Sakyo-ku, Kyoto-shi, Kyoto, 606-8501, Japan.
authors.forename: Akihiko
authors.initials: A
authors.lastname: Ishihara
authors.affiliation: Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Suma-ku, Kobe-shi, Hyogo, 654-0142, Japan. fujino@phoenix.kobe-u.ac.jp.
authors.forename: Hidemi
authors.initials: H
authors.lastname: Fujino
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects; D003094:Collagen / Q000378:metabolism; D005355:Fibrosis / Q000188:drug therapy / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism; D058628:Myofibroblasts / Q000187:drug effects / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D000072105:Superoxide Dismutase-1 / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D024341:Xanthophylls / Q000494:pharmacology
chemical_list: D000199:Actins; D000975:Antioxidants; D017382:Reactive Oxygen Species; D053773:Transforming Growth Factor beta1; D024341:Xanthophylls; C005948:astaxanthine; D003094:Collagen; D000072105:Superoxide Dismutase-1
keywords: Astaxanthin; Immobilization; Reactive oxygen species; Skeletal muscle fibrosis; Transforming growth factor-β1