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2019 Fiscal Year Final Research Report

Therapeutic strategy for diabetic microcirculatory disorder using transcutaneous carbon dioxide absorption combined pulsed ultrasonic irradiation

Research Project

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Project/Area Number 16H03208
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Rehabilitation science/Welfare engineering
Research InstitutionNagoya Women's University

Principal Investigator

Kondo Hiroyo  名古屋女子大学, 健康科学部, 准教授 (50333183)

Co-Investigator(Kenkyū-buntansha) 藤野 英己  神戸大学, 保健学研究科, 教授 (20278998)
石原 昭彦  京都大学, 人間・環境学研究科, 教授 (90184548)
Project Period (FY) 2016-04-01 – 2019-03-31
Keywords微小循環 / 代謝 / 糖尿病 / 二酸化炭素 / 血流 / 毛細血管
Outline of Final Research Achievements

Chronic hyperglycemia exposure caused a decrease in citrate synthase activity and regression of capillary network in skeletal muscle. Carbon absorption suppressed the decline of citrate synthase activity and capillary regression due to hyperglycemia and suppressed blood glucose rise. Furthermore, the expression levels of eNOS, PGC-1α, COX IV, and VEGF proteins related to metabolism and angiogenesis were increased and the expression level of angiogenesis inhibitor (TSP-1) was decreased in skeletal muscle. Pulsed ultrasound irradiation increased phosphorylation of integrin/focal adhesion kinase (FAK) and decrease phosphorylation of p38MAPK in myotubes induced inflammation. The irradiation also reduced the expression of inflammatory cytokines. These results indicated that percutaneous absorption of carbon dioxide and pulsed ultrasound therapy could be an effective intervention against microangiopathy induced by diabetes.

Free Research Field

応用健康科学 リハビリテーション科学 運動生理学

Academic Significance and Societal Importance of the Research Achievements

これらの研究結果から経皮的二酸化炭素吸収は,微小血管におけるずり応力とeNOS発現を増加させ,骨格筋の代謝や血管新生因子の増加と血管新生抑制因子の低下を引き起こし,高血糖曝露による骨格筋の酸化的リン酸化の機能低下や毛細血管退行を抑制することを明らかにした.また,パルス超音波照射はp38MAPKのリン酸化を抑制することで炎症を軽減させることが観察された.本研究成果から経皮的炭酸ガス吸収とパルス超音波による糖尿病性微小循環障害の予防改善への可能性が示された.

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Published: 2021-02-19  

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