糖化ストレスによる骨治癒遅延メカニズムの解明と新規治療薬の開発

Material type: 文書・図像類

Author: 松原, 秀憲ほか

Publisher: 金沢大学医薬保健研究域医学系

Publication date: 2019-06-17

Material Format: Digital

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Note (General)：: 糖尿病マウスにPyrを経口投与(2 mg/ml)した群(DM+Pyr)と非投与群(DM)，対照のPyr 投与群(CNT+Pyr)で実験を行った．左大腿骨遠位部に0.9 mmのドリルを用いて骨欠損を作成し, 骨欠損部の修復過程を3,7,10,14日目にCT 撮影で評価した．DM+Pyr群でCT値は修復...

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https://kaken.nii.ac.jp/search/?qm=10507057

https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K10896/

https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-16K10896/16K10896seika/

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Material Type: 文書・図像類
Title: 糖化ストレスによる骨治癒遅延メカニズムの解明と新規治療薬の開発
Author/Editor: 松原, 秀憲
Mmatsubara, Hidenori
Author Heading: 松原, 秀憲
Mmatsubara, Hidenori
Publication, Distribution, etc.: 金沢大学医薬保健研究域医学系
Publication Date: 2019-06-17
Publication Date (W3CDTF): 2019-06-17
Alternative Title: Revealing mechanism of delayed bone union by glycation stress and development new drug
Periodical title: 平成30(2018)年度科学研究費補助金基盤研究(C) 研究成果報告書 = 2018 Fiscal Year Final Research Report
No. or year of volume/issue: 2016-04-01 - 2019-03-31
Volume: 2016-04-01 - 2019-03-31
Pages: 4p.-
Text Language Code: jpn
Subject Heading: 骨癒合遅延
AGE
ピリドキサミン
糖尿病
Target Audience: 一般
Note (General): 糖尿病マウスにPyrを経口投与(2 mg/ml)した群(DM+Pyr)と非投与群(DM)，対照のPyr 投与群(CNT+Pyr)で実験を行った．左大腿骨遠位部に0.9 mmのドリルを用いて骨欠損を作成し, 骨欠損部の修復過程を3,7,10,14日目にCT 撮影で評価した．DM+Pyr群でCT値は修復過程早期の3,7日目でDM群よりも優位に上昇していた．MC3T3細胞を用いてAGEsの一種であるメチルグリオキサール(MGO)(1mM)含有の培地にPyr(,3mM)を添加し，ALP assayを行い，評価を行った．MGOによるMC3T3細胞のALP活性の低下はPyr (3mM)で改善が見られた．
Advanced glycation end-products (AGE) are implicated in diabetic complications. Pyridoxamine (PM) is one of the natural forms of vitamin B6 and is known to inhibit reactive carbonyl intermediates in AGE formation. In this study, we examined whether Metylglyoxal (MGO) was a cause of disturbed bone healing in diabetes and the bone problem was improved by PM treatment. We found that MGO could cause impaired osteoblastic differentiation and delayed bone repair in diabetes. For it, we employed PM in this study. PM treatment did not show any significant effects on blood glucose control. However, the delayed bone healing in diabetes was significantly improved by PM treatment from an early repair stage of day 7. In vitro cellular assays, MGO could inhibit the osteoblastic differentiation of MC3T3 cells. By adding PM, the ALP activity of ST2 cells was not substantially improved at 0.3 mM, but it was not complete at 1 mM, but it was improved.
研究課題/領域番号:16K10896, 研究期間(年度):2016-04-01 - 2019-03-31
出典：研究課題「糖化ストレスによる骨治癒遅延メカニズムの解明と新規治療薬の開発」課題番号16K10896（KAKEN：科学研究費助成事業データベース（国立情報学研究所））（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-16K10896/16K10896seika/)を加工して作成
DOI: 10.24517/00054595
Source: https://kanazawa-u.repo.nii.ac.jp/?action=repository_action_common_download&item_id=48273&item_no=1&attribute_id=26&file_no=1
https://kanazawa-u.repo.nii.ac.jp/?action=repository_action_common_download&item_id=48273&item_no=1&attribute_id=26&file_no=1
Access Restrictions: 限定公開
Rights (production): CC BY-NC-ND
Related Material: https://kaken.nii.ac.jp/search/?qm=10507057
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K10896/
https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-16K10896/16K10896seika/
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 金沢大学 : 金沢大学学術情報リポジトリKURA