JP2015531664A - 生体組織の治療のための方法及びシステム - Google Patents
生体組織の治療のための方法及びシステム Download PDFInfo
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Abstract
Description
用語「心臓組織の損傷」、「心臓組織の傷害」、及び「心血管組織の損傷」は、本明細書において互換的に使用され、心外膜、心内膜、及び/又は心筋の損傷を含む疾病、疾患、傷害又は損傷によって引き起こされた心血管系又は心臓内の任意の異常な組織の領域を意味し、含む。心血管組織損傷の原因の例としては、急性又は慢性ストレス(全身性高血圧、肺高血圧症、弁機能障害等)、冠動脈不全、虚血又は梗塞、炎症性疾患及び心筋症が含まれるがこれらに限定されない。
から選択される抗炎症剤を含む。アルクロフェナク、ジプロピオン酸アルクロメタゾン、アルゲストンアセトニド、アルファアミラーゼ、アムシナファル、アムシナフィド、アンフェナクナトリウム、アミプリロース塩酸塩、アナキンラ、アニロラク、アニトラザフェン、アパゾン、バルサラジド二ナトリウム、ベンダザック、ベノキサプロフェン、ベンジダミン塩酸塩、ブロメライン、ブロペラモール、ブデソニド、カルプロフェン、シクロプロフェン、シンタゾン、クリプロフェン、プロピオン酸クロベタゾール、酪酸クロベタゾン、クロピラク、プロピオン酸クロチカゾン、コルメタゾンアセテート、コルトドキソン、デカン酸塩、デフラザコート、デラテストリル、デポテストステロン、デソニド、デスオキシメタゾン、デキサメタゾンジプロピオネート、ジクロフェナクカリウム、ジクロフェナクナトリウム、二酢酸ジフロラゾン、ジフルミドンナトリウム、ジフルニサル、ジフルプレドナート、ジフタロン、ジメチルスルホキシド、ドロシノニド、エンドリソン、エンリモマブ、エノリカムナトリウム、エピリゾール、エトドラク、エトフェナマート、フェルビナク、フェナモール、フェンブフェン、フェンクロフェナク、フェンクロラク、フェンドサール、フェンピパロン、フェンチアザク、フラザロン、フルアザコルト、フルフェナム酸、フルミゾール、フルニソリド酢酸、フルニキシン、フルニキシンメグルミン、フルオコルチンブチル、フルオロメトロン酢酸塩、フルクァゾン、フルルビプロフェン、フルレトフェン、プロピオン酸フルチカゾン、フラプロフェン、フロブフェン、ハルシノニド、ハロベタゾールプロピオン酸、酢酸ハロプレドン、イブフェナク、イブプロフェン、イブプロフェンアルミニウム、イブプロフェンピコノール、イロニダップ、インドメタシン、インドメタシンナトリウム、インドプロフェン、インドキソール、イントラゾール、イソフルプレドン酢酸、イソキセパク、イソキシカム、ケトプロフェン、塩酸ロフェミゾール、ロモキシカム、エタボン酸ロテプレドノール、メクロフェナム酸ナトリウム、メクロフェナム酸、メクロリゾンジブチレート、メフェナム酸、メサラミン、メセクラゾン、メステロロン、メタンドロステノロン、メテノロン、メテノロン酢酸エステル、スレプタン酸メチルプレドニゾロン、モミフルマート、ナブメトン、ナンドロロン、ナプロキセン、ナプロキセンナトリウム、ナプロキソール、ニマゾン、オルサラジンナトリウム、オルゴテイン、オルパノキシン、オキサンドロロン、オキサプロジン、オキシフェンブタゾン、オキシメトロン、パラニリン塩酸塩、ペントサンポリ硫酸ナトリウム、フェンブタゾンナトリウムグリセラート、ピルフェニドン、ピロキシカム、ケイ皮酸ピロキシカム、ピロキシカムオラミン、ピルプロフェン、プレドナザート、プリフェロン、プロドール酸、プロカゾン、プロキサゾール、プロキサゾールクエン酸塩、リメキソロン、ロマザリット、サルコレクス、サルナセジン、サルサレート、サンギナリウムクロリド、セクラゾン、セルメタシン、スタノゾロール、スドキシカム、スリンダク、スプロフェン、タルメタシン、タルニフルマート、タロサラート、テブフェロン、テニダップ、テニダップナトリウム、テノキシカム、テシカム、テシミド、テストステロン、テストステロンブレンド、テトリダミン、チオピナク、チクソコルトールピバル酸エステル、トルメチン、トルメチンナトリウム、トリクロニド、トリフルミダート、ジドメタシン、及びゾメピラックナトリウム
当技術分野で知られるように、スタチンは、主に、肝臓におけるコレステロール産生のレベルを低下させるように機能する薬剤の一群である。コレステロールのより低いレベルは、コレステロール生合成経路のメバロン酸の産生を制限するスタチンによって達成される。スタチンは、拮抗的にHMG−CoA還元酵素を阻害し、分子が非常に似ているので、スタチンがコレステロール生合成経路でHMG−CoA還元酵素に実際に取って替わり、メバロン酸が生成される速度を減少させ、続いて肝臓でコレステロールが生成される速度を減少させる。
スタチンは、血管壁細胞、及び心血管系への多数の追加的な望ましい影響も有する。これの1つの具体例は、トロンボキサンA2(TXA2)である。スタチンはTXA2の低減を助けることができ、ひいては心血管系における血小板活性化を低下させる。
減少したMMP及び減少したTFはプラークの安定性の増大にもつながり、このことは、プラークの部分が破裂してより小さい管内で詰まる可能性を減少させることにより、脳卒中又は心筋梗塞を予防することに役立つ場合がある。プラークの安定性はさらに、アテローム性動脈硬化を減少させることに役立つ。
RhoA活性化の阻害は又、組織プラスミノーゲン活性化因子(t‐PA)及びプラスミノーゲン活性化抑制因子1型(PAI‐1)の存在に影響を与える。T‐PAは、血餅の分解に関与するタンパク質であり、内皮細胞に見出される。それは酵素としてプラスミノーゲンのプラスミン、血餅の分解(線溶)に関与する主要な酵素への変換を触媒する。
RhoA活性化の阻害は又、心血管系における一酸化窒素(NO)の存在に影響を与える。内皮は周囲の平滑筋にリラックスさせるシグナルを送るためにNOを使い、そのことにより血管が拡張し血流が増大する。NOは、血管平滑筋の収縮及び成長、血小板凝集、及び内皮への白血球接着を抑制することにより、血管の恒常性に寄与する。それらの因子は、典型的にはスタチンの投与で典型的であるような方法で調節されるとき、NOが内皮機能不全の低減に役立つことを可能にするものである。白血球接着の減少は、細胞外マトリックスとともに局所的にともに投与されるとき、スタチンに関連するNOの産生がどのように望ましい炎症の低減に役立つかの具体的な例である。
スタチンの投与は、エンドセリン及びアンジオテンシン受容体の存在に作用し得る。エンドセリン及びアンジオテンシン受容体は又、スタチン投与に関連する次のRhoA活性化の阻害により影響され得る。
C反応性タンパク質(CRP)もスタチン投与によって影響を受ける。CRPは、血液中に見いだされ、それらのレベルは炎症のレベルの差異に応じて逸脱する。CRPレベルは、スタチンの投与に応じて減少する。このことは、スタチンが炎症の低減に与える影響の結果として機能する。
接着分子は、細胞の表面に位置し、炎症及び血管内皮細胞におけるトロンビン形成に関連するタンパク質である。炎症のより多い発生は、細胞接着分子のより多い発生を伴う。スタチンは、内皮上の接着分子の存在を減少させるように機能する。このことは、白血球及びその後のプラークの付着に係る付着機構を除去することによって炎症を軽減するのに役立ち、その結果、アテローム性動脈硬化の機会を低下させる。
Rac‐1は、ヒトの細胞に見いだされるタンパク質である。それは、内皮細胞遊走、細管形成、付着性、透過性において中心的な役割を果たす。Rac‐1の発現は、スタチンの投与に影響される場合があり、具体的に、スタチンによってRac‐1が減少する。Rac‐1の存在が減少することは又、活性酸素種(ROS)の減少をもたらす。ROSは、細胞シグナル伝達及び恒常性において重要な役割を有する化学反応性分子である。
・損傷した生体組織、特に、新血管組織に送達されたときに、新血管形成を誘導し、損傷した心血管組織の生存及び再生を促進する薬理組成物の提供すること。
・損傷した生体組織、特に、新血管組織に送達されたときに、宿主組織の増殖、バイオリモデリング、及び部位特異的な構造的及び機能的特性を有する心血管組織構造の再生を誘導する細胞外マトリックス(ECM)組成物を提供すること。
・薬理組成物、特に、ECM組成物を損傷した又は罹患した生体組織に直接に投与するための改良された方法及びシステムを提供すること。
Claims (3)
- 損傷した生体組織を治療するための組成物であって、
細胞外マトリックス(ECM)足場成分および生物活性成分を有するECM組成物を有してなり、前記ECM足場成分は中皮からなり、前記生物活剤成分はスタチンを含む、組成物。 - 前記ECM組成物が、水及び生理食塩水から成る群から選択される流動化成分を含むことを特徴とする請求項1に記載の組成物。
- 前記スタチンが、アトルバスタチン、セリバスタチン、フルバスタチン、ロバスタチン、メバスタチン、ピタバスタチン、プラバスタチン、ロスバスタチン、及びシンバスタチンから成る群から選択されることを特徴とする請求項1に記載の組成物。
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