| 廖文筠,张莹莹,陈睦虎,等.辅酶 Q10对脓毒血症休克大鼠血管平滑肌细胞功能的影响[J].安徽医药,2022,26(8):1500-1504. |
| 辅酶 Q10对脓毒血症休克大鼠血管平滑肌细胞功能的影响 |
| Effect of coenzyme Q10 on function of vascular smooth muscle cell in rats with septic shock |
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| DOI：10.3969/j.issn.1009-6469.2022.08.004 |
| 中文关键词: 休克，脓毒性 辅酶 Q10 血管平滑肌细胞 氧化应激 α-肌动蛋白 |
| 英文关键词: Shock, septic Coenzyme Q10 Vascular smooth muscle cells Oxidative stress α-actin |
| 基金项目:西南医科大学省厅级青年基金资助项目( 0903-00031063)；泸州市科技局创新苗子资助项目( 17254) |
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| 中文摘要: |
| 目的探讨辅酶 Q10对脓毒血症休克大鼠血管平滑肌细胞功能的影响及其作用机制研究。方法采用 SD大鼠尾静脉注射脂多糖( LPS)的方法建立脓毒症休克动物模型，分离取出主动脉， 0.2%胶原酶消化分离平滑肌细胞( SMCs)，自然纯化及差速贴壁纯化血管平滑肌细胞，将分离后的 SMC分别接种到 96孔板中，分为 4组，分别为正常对照组、正常对照组 +辅酶 Q10、LPS组、 LPS+辅酶 Q10组，分别检测 4组的增殖和氧化应激产物产生情况，在 6、12、24、48 h后分别检测正常对照组、正常对照组 +辅酶 Q10、LPS组、 LPS+辅酶 Q10组 SMCs丙二醛水平，在 48 h后检测 α-肌动蛋白( α-actin)、骨桥蛋白( OPN)的相对表达量。结果随时间推移， LPS组中 SMC细胞凋亡和氧化应激产物均较正常对照组增多，在 48 h时达到峰值，分别增多 11.4倍和 5.6倍； LPS+辅酶 Q10组中氧化应激产物较 LPS组减少近 50%；在 48 h时辅酶 Q10在正常培养环境下对 SMC的 α-actin、OPN蛋白的相对表达量差异无统计学意义( P>0.05)，而对脓毒症休克 SD大鼠分离的 SMC可以明显减低氧化应激产物的生成及上调 α-actin蛋白的相对表达量近 1.57倍，下调 OPN蛋白的相对表达量 1.17倍。结论由 LPS所致的脓毒症休克的发病机制与血管中膜平滑肌细胞表型改变密切相关，辅酶 Q10可明显减低氧化应激产物的生成及上调 α-actin蛋白的相对表达量，缓解了因 LPS所致脓毒血症休克的血管病理化转变。收缩型平滑肌细胞是正常情况下血管壁的重要组成部分，而疾病病理血管则表现为合成型，为脓毒血症休克的病理性血管形成提供理论基础。 |
| 英文摘要: |
| Objective To investigate the effect of coenzyme Q10 on the function of vascular smooth muscle cell (VSMC) in septic rats and its mechanisms.Methods An animal model of sepsis shock was established by tail vein injection of endotoxin lipopolysaccha-ride (LPS). The aorta from SD rat was separated and smooth muscle cells were isolated with collagenase. The cells were collected by themethod of natural purification and purification of sticking wall at different speed. The proliferation and oxidative stress production wasrespectively detected by enzyme standard instrument in four groups, including control group, control group + coenzyme Q10, LPSgroup, LPS group + coenzyme Q10. The concentration of malondialdehyde (MDA) was detected at 6,12,24,48 h.The protein expressionof α-SM-actin and OPN was detected after 48 h.Results Compared with the control group, the number of cell apoptosis and oxidativestress production in the LPS group, peaking at 48 h, were increased by 11.4 times and 5.6 times, respectively; on the contrary, com-pared with LPS group, the oxidative stress production were reduced nearly 50% in LPS group + coenzyme Q10; In control group, Theprotein expression of α-SM-actin and OPN had no statistical differences in VSMC treated with coenzyme Q10 at 48 h (P>0.05). In LPS group, the protein expression of α-SM-actin obviously increased 1.57 times in VSMC treated with coenzyme Q10 at 48 h, except for theprotein expression of OPN decreasing 1.17 times.Conclusions The pathogenesis of sepsis shock caused by lipopolysaccharide (LPS)is closely related to phenotypic changes of vascular smooth muscle cell; Coenzyme Q10 can significantly reduce the production of oxida-tive stress products and increase the relative expression of α-actin protein, and alleviate the vascular pathological transformation of sep-sis shock caused by LPS. Constrictive smooth muscle cells are an important part of the vascular wall under normal conditions, while dis-ease pathological blood vessels are shown as synthetic, which provides a theoretical basis for pathological vascular formation in sepsisshock. |
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