Results: K-115 significantly inhibited VEGF-induced HRVECs
migration (26.2% reduction at 3mM, 43.2% reduction at 30mM,
P<0.01 respectively) and proliferation (39.5% reduction at
3mM, 45.1% reduction at 30mM, P<0.05 respectively) in a dosedependent
manner. Tight junction proteins (occluding, claudin)
were disassembled from intercellular junctions in VEGF simulated
HRVECs, and this was tended to prevented with K-115 pretreatment.
In the K-115 eye drop-treated mice, the areas of neovascularization
in the flat-mount retina showed a significant reduction compared to
those of the vehicle-treated mice (41.8% reduction at 0.4% K-115,
47.3% reduction at 0.8% K-115, P<0.01 respectively). Moreover,
K-115 eye drops significantly reduced the areas of avascular
retina in a dose-dependent manner (23% reduction at 0.4% K-115,
41.9% reduction at 0.8% K-115, P<0.01 respectively). The areas of
fluorescein leakage were also significantly reduced in 0.8% K-115-
treated mice compared with vehicle-treated mice (58.4% reduction,
P<0.05).
Conclusions: Topical K-115 treatment has the potential to become a
novel therapeutic strategy in the treatment of diabetic retinopathy.
Results: K-115 significantly inhibited VEGF-induced HRVECs
migration (26.2% reduction at 3mM, 43.2% reduction at 30mM,
P<0.01 respectively) and proliferation (39.5% reduction at
3mM, 45.1% reduction at 30mM, P<0.05 respectively) in a dosedependent
manner. Tight junction proteins (occluding, claudin)
were disassembled from intercellular junctions in VEGF simulated
HRVECs, and this was tended to prevented with K-115 pretreatment.
In the K-115 eye drop-treated mice, the areas of neovascularization
in the flat-mount retina showed a significant reduction compared to
those of the vehicle-treated mice (41.8% reduction at 0.4% K-115,
47.3% reduction at 0.8% K-115, P<0.01 respectively). Moreover,
K-115 eye drops significantly reduced the areas of avascular
retina in a dose-dependent manner (23% reduction at 0.4% K-115,
41.9% reduction at 0.8% K-115, P<0.01 respectively). The areas of
fluorescein leakage were also significantly reduced in 0.8% K-115-
treated mice compared with vehicle-treated mice (58.4% reduction,
P<0.05).
Conclusions: Topical K-115 treatment has the potential to become a
novel therapeutic strategy in the treatment of diabetic retinopathy.
結果:
用量依存的に投与されたK-115により、HRVEC移動(3mMの26.2%の縮小、30mMの43.2%の縮小、P、それぞれ<0.01)および増殖(3mMの39.5%の縮小、30mMの45.1%の縮小、P、それぞれ<0.05)は著しく抑制された。
密着結合タンパク質(咬み合って、claudin)はVEGFの中の細胞間結合から逆アセンブルされました、HRVECとこれをシミュレートした、向かわれた、K-115前処理で防がれました。
K-115点眼薬を投与したハツカネズミでは、平面マウント網膜中の新血管新生のエリアは、食塩水を投与したハツカネズミのものと比較して、著しい減少を示しました。(0.4%のK-115投与は41.8%の縮小、0.8%のK-115投与は47.3%の縮小、P、それぞれ<0.01)
さらに、K-115点眼薬の用量依存的なやり方で血管がない網膜のエリアを著しく縮小しました。(0.4%のK-115の23%の縮小、0.8%のK-115の41.9%の縮小、P、それぞれ<0.01)
フルオレスセイン漏出のエリアも、食塩水を投与したハツカネズミと比較して、0.8%のK-115を投与したハツカネズミでは著しく縮小しました(58.4%の縮小およびP<0.05)。
結論:
話題のK-115治療には糖尿病性網膜症の治療での新しい治療方針になる可能性があります。
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