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论著·基础研究 | 更新时间:2025-02-27
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Col003对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖和迁移的影响
Effect of Col003 on proliferation and migration of vascular smooth muscle cells induced by angiotensin Ⅱ

广西医学 页码:72-76

作者机构:邓梦雨,硕士,医师,研究方向为缺血性脑卒中。

基金信息:国家自然科学基金(8216050094);广西自然科学基金(2023GXNSFDA026017)

DOI:10.11675/j.issn.0253⁃4304.2025.01.13

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目的 探讨Col003对血管紧张素Ⅱ(AngⅡ) 诱导的血管平滑肌细胞(VSMCs)增殖和迁移的影响。方法 (1)体外培养VSMCs,给予不同浓度(25 μmol/L、37.5 μmol/L、50 μmol/L、62.5 μmol/L、75 μmol/L)Col003处理后,采用乳酸脱氢酶法检测细胞毒性,筛选Col003的干预浓度。(2)体外培养VSMCs,给予不同浓度(0.01 μmol/L、0.1 μmol/L、1 μmol/L、10 μmol/L)AngⅡ处理后,采用CCK⁃8法检测细胞增殖活性,筛选AngⅡ诱导VSMCs增殖的最佳浓度。(3)将VSMCs分为空白对照组(给予细胞培养基处理)、AngⅡ组(给予1 μmol/L AngⅡ处理)、AngⅡ+溶剂对照组(给予1 μmol/L AngⅡ+二甲基亚砜处理)、AngⅡ+25 μmol/L Col003组(给予1 μmol/L AngⅡ+25 μmol/L Col003处理)、AngⅡ+37.5 μmol/L Col003组(给予1 μmol/L AngⅡ+37.5 μmol/L Col003处理)、AngⅡ+阿托伐他汀组(给予1 μmol/L AngⅡ+阿托伐他汀处理),分别采用CCK⁃8法和划痕试验评估Col003对AngⅡ诱导的VSMCs增殖和迁移的影响。结果 筛选出Col003干预浓度为25 μmol/L和37.5 μmol/L,AngⅡ干预浓度为1 μmol/L。与AngⅡ组相比,AngⅡ+25 μmol/L Co1003组、AngⅡ+37.5 μmol/L Co1003 组、AngⅡ+阿托伐他汀组的细胞存活率降低(P<0.05),AngⅡ+37.5 μmol/L Co1003 组、AngⅡ+阿托伐他汀组的划痕汇合率降低(P<0.05)。与AngⅡ+37.5 μmol/L Col003组相比,AngⅡ+阿托伐他汀组的细胞存活率和划痕汇合率差异无统计学意义(P>0.05)。结论 Col003可以抑制AngⅡ诱导的VSMCs增殖与迁移,可能具有潜在的抗动脉粥样硬化作用。

Objective To explore the effect of Col003 on proliferation and migration of vascular smooth muscle cells (VSMCs) induced by angiotensin Ⅱ(AngⅡ). Methods (1) VSMCs were cultured in vitro, after different concentrations of Col003 (25 μmol/L, 37.5 μmol/L, 50 μmol/L, 62.5 μmol/L, 75 μmol/L) treatment, cytotoxicity was detected by employing the lactate dehydrogenase method for screening intervention concentration of Col003. (2) VSMCs were cultured in vitro, after different concentrations of AngⅡ (0.01 μmol/L, 0.1 μmol/L, 1 μmol/L, 10 μmol/L) treatment, cell proliferation activity was detected by using the CCK⁃8 method for screening the optimal concentration of VSMCs proliferation induced by AngⅡ. (3) VSMCs were assigned to blank control group (receiving cell culture medium for treatment), AngⅡ group (receiving 1 μmol/L AngⅡ for treatment), AngⅡ+solution control group (receiving 1 μmol/L AngⅡ+dimethyl sulfoxide for treatment), AngⅡ+25 μmol/L Col003 group (receiving 1 μmol/L AngⅡ+25 μmol/L Col003 for treatment), AngⅡ+37.5 μmol/L Col003 group (receiving 1 μmol/L AngⅡ+37.5 μmol/L Col003 for treatment), or AngⅡ+atorvastatin group (receiving 1 μmol/L AngⅡ+atorvastatin for treatment). The effect of Col003 on AngⅡ⁃induced VSMCs proliferation and migration was evaluate by employing the CCK⁃8 method and scratch test. Results The intervention concentrations of Col003 screened were 25 μmol/L and 37.5 μmol/L, and of AngⅡ screened was 1 μmol/L. Compared with the AngⅡ group, the AngⅡ+25 μmol/L Co1003 group, the AngⅡ+37.5 μmol/L Co1003 group, and the AngⅡ+atorvastatin group exhibited a decreased cell survival rate (P<0.05); furthermore, the AngⅡ+37.5 μmol/L Co1003 group and the AngⅡ+atorvastatin group yielded decreased scratch convergence rate (P<0.05). Compared with the AngⅡ+37.5 μmol/L Col003 group, there was no statistically significant difference in cell survival rate and scratch convergence rate of the AngⅡ+atorvastatin group (P>0.05). Conclusion Col003 can inhibit the proliferation and migration of AngⅡ⁃induced VSMCs, which may have potential anti⁃atherosclerosis effect.

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