| 张芬,戴耕武,杨镓宁,等.氢化可的松局部注射加 90Sr-90Y同位素敷贴抑制大鼠皮肤瘢痕形成机制分析[J].安徽医药,2021,25(9):1885-1888. |
| 氢化可的松局部注射加 90Sr-90Y同位素敷贴抑制大鼠皮肤瘢痕形成机制分析 |
| Analysis of the mechanism of hydrocortisone local injection plus 90Sr-90Y isotope application in inhibiting skin scar formation in rats |
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| DOI：10.3969/j.issn.1009-6469.2021.09.045 |
| 中文关键词: 瘢痕 氢化可的松 放疗 Smad3 转化生长因子 -β1 转化生长因子激活激酶 1 90Sr-90Y敷贴放射治疗 大鼠， Sprague-Dawley 明显， |
| 英文关键词: Cicatrix Hydrocortisone Radiotherapy Smad3 TGF-β1 TAK1 Radionuclide applicator therapy Rats,Sprague-Dawley |
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| 中文摘要: |
| 目的探索氢化可的松局部注射加放疗抑制皮肤瘢痕形成的效果及机制。方法首先制备 30只 SD大鼠瘢痕模型，并采用随机数字表法分为对照组、糖皮质激素组、糖皮质激素 +放疗组，每组各 10只；对照组不采取任何治疗措施，糖皮质激素组采用 2.5%醋酸氢化可的松注射液( 25 g/L)注射治疗，共 2个疗程，糖皮质激素 +放疗组采用 2.5%醋酸氢化可的松注射液( 25 g/L)局部注射联合 90Sr-90Y敷贴放疗的方法，共 2个疗程，两组均从术后第 14天开始采取治疗措施，治疗过程中，每天记录瘢痕的长度、宽度及是否产生增生的变化；术后第 30天，将大鼠杀死，取瘢痕组织，并通过蛋白质印迹法测量瘢痕组织中 Smad3蛋白表达水平，酶联免疫吸附测定( ELISA)检测瘢痕组织中转化生长因子 -β1(TGF-β1)和转化生长因子激活激酶 1(TAK1)的表达水平。结果手术后第 29天，对照组的瘢痕长度为( 18.55±2.31)mm，宽度为( 7.3±1.13)mm，80%出现了瘢痕增生；糖皮质激素组的瘢痕长度为( 15.39±2.17)mm，宽度为( 4.7±1.25)mm，60%出现了瘢痕增生；糖皮质激素 +放疗组的瘢痕长度为( 10.47±1.92)mm，宽度为(1.3±0.94)mm，20%出现了瘢痕增生。糖皮质激素 +放疗组的瘢痕长宽显著小于对照组及糖皮质激素组(均 P <0.001)瘢痕增生水平明显轻于对照组及糖皮质激素组( P<0.05)。蛋白质印迹法发现，糖皮质激素 +放疗组的 Smad3蛋白表达水平低于对照组及糖皮质激素组(均 P<0.05)。 ELISA法测定 TGF-β1和 TAK1发现，糖皮质激素 +放疗组 TGF-β1和 TAK1的表达水平分别明显低于对照组及糖皮质激素组(均 P<0.05)。结论氢化可的松局部注射联合放疗可通过下调 Smad3途径及 TGF-β1和 TAK1途径抑制瘢痕的形成，效果明显。 |
| 英文摘要: |
| Objective To explore the effect and mechanism of hydrocortisone local injection plus radiotherapy in inhibiting skin scar formation.Methods SD rat models of scar were established and assigned into control group, glucocorticoid group, and glucocorticoid plus radiotherapy group by random number table method, 10 in each group. No control measures were taken in the control group,2.5% hydrocortisone acetate injection (25 g/L) was carried out with 2 courses in the glucocorticoid group, and 2.5% hydrocortisone acetate injection (25 g/L) local injection combined with 90Sr-90Y application radiotherapy were carried out with 2 courses in glucocorticoidplus radiotherapy group. These two groups both started their respective treatments from the 14th day after surgery. During the treatment, the length and width of the scar and whether hyperplasia occurred were recorded every day. On the 30th day after surgery, therats were sacrificed, the scar tissue was taken, and the expression level of Smad3 protein in the scar tissue was measured by Western Blot analysis. The expression levels of transforming growth factor-β1 (TGF-β1) and transforming growth factor-β activated kinase-1 (TAK1) in the scar tissue were determined by enzyme linked immunosorbent assay (ELISA).Results On the 29th day after surgery,the length and width of the scar in the control group were (18.55±2.31) mm,(7.3±1.13)mm, respectively, and hypertrophic scarsaccounted for 80%; the length and width of the scar in the glucocorticoid group were (15.39±2.17) mm, (4.7±1.25)mm,respectively, and hypertrophic scars accounted for 60%; the length and width of the scar in the glucocorticoid plus radiotherapy group were (10.47±1.92) mm,(1.3±0.94) mm, respectively, and hypertrophic scars accounted for 20%. The scar length and width of the glucocorticoid plus radiotherapy group were significantly smaller than those of the control group and glucocorticoid group (both P<0.001), and the scar hypeplasia was lighter (P<0.05). Western blot analysis showed that the expression level of Smad3 protein in the glucocorticoid plus radiotherapygroup was significantly lower than those of the control group and glucocorticoid group (both P<0.05). ELISA assay for TGF-β1 and TAK1 found that the expression levels of TGF-β1 and TAK1 in the glucocorticoid plus radiotherapy group were significantly lower thanthose in the control group and glucocorticoid group (both P<0.05).Conclusion Hydrocortisone local injection combined with radiotherapy can inhibit the formation of scar by down-regulating the Smad3 pathway and TGF-β1 and TAK1 pathways. |
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