| 李鹤,许志会,陈蕾,等.裸花紫珠通过激活转化生长因子 β1/Smad3信号通路介导的血管生成促进糖尿病足溃疡创面愈合[J].安徽医药,2026,30(5):906-913. |
| 裸花紫珠通过激活转化生长因子 β1/Smad3信号通路介导的血管生成促进糖尿病足溃疡创面愈合 |
| Callicarpa nudiflora promotes diabetic foot ulcer wound healing via activation of TGF-β1/Smad3 signaling pathway-mediated angiogenesis |
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| DOI：10.3969/j.issn.1009-6469.2026.05.012 |
| 中文关键词: 紫珠属 糖尿病足 裸花紫珠 TGF-β1/Smad3信号通路 血管生成 |
| 英文关键词: Callicarpa Diabetic foot Callicarpa nudiflora TGF-β1/Smad3 signaling pathway Angiogenesis |
| 基金项目:河北省中医药管理局科研计划项目( 2018232) |
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| 中文摘要: |
| 目的探讨裸花紫珠( CN)对糖尿病足溃疡(DFU)创面愈合的作用及机制。方法 2024年 1―6月，采用高糖(HG)诱导人脐静脉内皮细胞( HUVECs)及高脂高糖饲养联合链脲佐菌素( STZ)腹腔注射 Sprague-Dawley(SD)大鼠构建糖尿病细胞和动物模型，剪掉大鼠右侧后脚背面部分皮肤构建糖 DFU模型。分别采用高、中、低三个剂量的裸花紫珠处理细胞和动物。细胞计数试剂盒 -8(CCK-8)和细胞计数实验检测细胞增殖情况。划痕和迁移侵袭实验( Transwell)评价细胞迁移能力。成管实验检测细胞血管生成能力。蛋白质印迹法、免疫荧光和免疫组化染色检测蛋白表达情况。苏木精 -伊红染色( HE)染色评价组织病理学改变。结果 CN剂量 0、25、50、100、200 g/L细胞活力分别为( 100±1.63)%、(112.33±2.28)%、(122.07±3.39)%、(133.37± 4.73)%、(102.75±3.74)%，活细胞数分别为( 8.84±0.17)×103(9.79±0.19)×103(11.38±0.35)×103(12.62±0.39)×103(8.94±0.23)×103.025、50和 100 g/L的 CN明显提高 HUVECs活力和存活细胞数，而200g/L、的CN对HUVECs、的增殖无促进作用(F= |
| 英文摘要: |
| Objective To explore the effect and mechanism of Callicarpa nudiflora (CN) on the wound healing of diabetic foot ulcer (DFU).Methods From January 2024 to June 2024, high glucose (HG) induced human umbilical vein endothelial cells (HUVECs) toconstruct diabetic cell model, and high glucose and high lipid food combined with streptozotocin (STZ) intraperitoneal injection intosprague dawley (SD) rat to establish diabetic animal model, respectively. DFU was created by cutting off part of the skin layer on theback of the right hind foot of rats. High-, medium-and low-doses of CN were used for treatment of cells and animals, respectively. Cell counting kit-8 (CCK-8) and cell count were used for evaluation of cell proliferation. Cell migratory ability was measured by scratch andTranswell assays. The angiogenesis was assessed by tube forming assay. Western blotting, immunofluorescence and immunohistochem.istry staining were performed to determine protein expressions. Histopathological changes were detected by hematoxylin-eosin staining (HE) staining. Results The cell viability at the dosage of CN of 0, 25, 50, 100 and 200g/L were (100±1.63)% , (112.33±2.28)% ,(122.07±3.39)%, (133.37±4.73)%, (102.75±3.74)%, respectively, and the number of living cells were (8.84±0.17)×103, (9.79±0.19)× 103, (11.38±0.35)×103, (12.62±0.39)×103, (8.94±0.23)×103, respectively. 25, 50 and 100 g/L of CN significantly increased HUVECscell viability and live cells, while 200 g/L CN had no effect on HUVECs proliferation (F=34.33, P<0.001; F=369.35, P<0.001). There.fore, CN at 25, 50 and 100 g/L were selected for subsequent cell experiments. The migratory and angiogenesis abilities were significant.ly decreased in HG group compared with normal glucose group, and CN treatment promoted migration and angiogenesis of HUVECs ina dose-dependent manner. HG treatment significantly down-regulated the levels of cluster of differentiation 31 (CD31), vascular endo. thelial growth factor A (VEGF-A), transforming growth factor beta 1 (TGF-β1) and phosphorylated Smad3 (p-Smad3) in HUVECs, while CN attenuated the inhibition of HG on the expressions of those proteins mentioned above dose-dependently. In vivo experiment resultsshowed that the fasting blood glucose of the rats were all greater than 16.7 mmol/L at the 1st, 4th, 7th, 11th and 14th day of wound for.mation except for the control group, indicating that the model was successful, and CN could significantly reduce the fasting blood glu.cose content. The expression levels of CD31 in control group, DFU group, CN-L group, CN-M group and CN-H group were (2.70±0.46, 0.30±0.45, 1.20±0.40, 2.10±0.70, 2.60±0.49), the expression levels of VEGF-A were (2.80±0.40, 0.40±0.48, 1.50±0.50, 2.40±0.49, 2.70±0.46), the expression levels of TGF-β1 were (1.00±0.04, 0.21±0.03, 0.52±0.08, 0.86±0.07, 0.94±0.05), the expression levels of p-Smad3 were (1.00±0.05, 0.15±0.04, 0.26±0.06, 0.47±0.08, 0.82±0.08). Compared with the control group, the wound healing rate of ratsin DFU group was significantly slower, and the protein expressions of CD31, VEGF-A, TGF-β1 and p-Smad3 in wound and surrounding tissues were significantly decreased (F=35.62, P<0.001; F=41.85, P<0.001; F=308.70, P<0.001; F=281.90, P<0.001). CN accelerated wound healing and enhanced the levels of CD31, VEGF-A, TGF-β1 and p-Smad3.Conclusion CN promotes DFU wound healing by activating TGF-β1/Smad3 signaling pathway to promote angiogenesis. |
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