Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter.

Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter.
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祛瘀生肌方通过抑制前列腺素转运蛋白表达促进糖尿病伤口愈合

DOI:
10.1155/2021/8849935
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发表时间:
2021
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
通讯作者:
Ze K
Ze K
中科院分区:
其他
文献类型:
--
作者:
Lu Y;Ding X;Qi F;Ru Y;Kuai L;Chen S;Yang Y;Li X;Li F;Li B;Zhou M;Ze K

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祛瘀生肌方是临床上广泛应用的中药方剂,对糖尿病溃疡有较好的治疗效果。然而,QSF如何治疗糖尿病溃疡的潜在机制仍然是难以捉摸的。 目的:探讨QSF对糖尿病创面愈合不良的作用机制。 采用Db/db小鼠,观察QSF的治疗作用。通过苏木精和伊红(H&E)染色进行进一步的组织学分析。此外,前列腺素转运蛋白(PGT),前列腺素E2(PGE 2)和血管生成因子血管内皮生长因子(VEGF)的表达模式进行了评估,免疫染色(IHC)分析,ELISA测定,实时定量聚合酶链反应(RT-qPCR),和蛋白质印迹分析在体内。以人真皮微血管内皮细胞(Human dermal microvascular endothelial cells,HDMECs)为研究对象,采用shRNA干扰技术,观察QSF对HDMECs细胞迁移、前列腺素(PGT)、前列腺素E2(PGE 2)和血管生成因子VEGF的影响。 在db/db小鼠伤口上应用QSF显著加速伤口闭合。QSF治疗后PGT降低,PGE 2升高,血管生成因子VEGF水平升高。此外,QSF促进了HDMEC迁移。通过shRNA抑制PGT表达逆转QSF治疗的体外表型。 总之,我们的研究结果表明,QSF通过消除PGT的表达来改善糖尿病相关的伤口愈合缺陷。
Quyu Shengji Formula (QSF), a Chinese medicine formula widely used in the clinic, has proven therapeutic effects on diabetic ulcers. Nevertheless, the potential mechanism of how QSF cures diabetic ulcer remains elusive. To assess the mechanism of QSF against wound healing defects in diabetes. Db/db mice were adopted to determine the therapeutic potential of QSF. Further histology analysis was performed by hematoxylin and eosin (H&E) staining. Moreover, the expression patterns of prostaglandin transporter (PGT), prostaglandin E2 (PGE2), and angiogenesis factor vascular endothelial growth factor (VEGF) were evaluated by immunostaining (IHC) analysis, ELISA assay, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot analysis in vivo. Human dermal microvascular endothelial cells (HDMECs) and the shRNA interference technique were used to explore the effects of QSF on cell migration, PGT, PGE2, and angiogenesis factor VEGF in vitro. Applied QSF on the wound of db/db mice significantly accelerated wound closure. Reductions of PGT and elevations of PGE2 and increased angiogenesis factor VEGF levels were shown after QSF treatment in vivo and in vitro. Furthermore, QSF promoted HDMEC migration. Inhibition of the expression of PGT by shRNA reversed phenotypes of QSF treatment in vitro. Taken together, our findings reveal that QSF ameliorates diabetes-associated wound healing defects by abolishing the expression of PGT.
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