三七皂苷R1调节炎性T细胞亚群保护血管内皮的实验研究

目的探讨炎性T细胞亚群在胶原酶诱导的血管内皮损伤早期的变化状态及三七皂苷R1的保护作用机制。方法采用扫描电镜观察ApoE-/-小鼠动脉内皮损伤程度;流式细胞术检测小鼠外周血中CD62Phi、CD62P+CD62E+脱落内皮细胞的比例;胞内外因子染色法检测炎性T细胞亚群分泌TNF-α、IL-17的水平。结果扫描电镜下,内皮损伤模型组小鼠血管内膜受损明显,内皮脱落面积明显增加,实验组经三七皂苷R1处理后血管内皮偶有脱落(P均<0.05);另外,模型组脱落内皮细胞CD62Phi、CD62P+CD62E+比例明显高于正常对照组,同时,T细胞分泌TNF-α、IL-17的能力明显升高,而实验组脱落内皮细胞比例明显低于模型组,T细胞分泌IL-17的比例下降(P均<0.05)。结论 Th17细胞亚群比例升高与血管内皮早期损伤密切相关,三七皂苷R1在保护血管内皮的同时,可选择性地下调Th17细胞亚群比例。

Regulation of sanchinoside R1 on inflammatory T lymphocytes in protecting vascular endothelium lesion in ApoE-/- mice

Aim To explore the protective mechanisms of sanchinoside R1 on inflammatory T-cell subsets in collagenase Ⅱ-induced vascular endothelium lesion.Methods The morphological changes of endothelium in ApoE-/-mice were observed by scanning electron microscope.Flow cytometry was used to analyze the expressions of CD62P,CD62E of disrupted endothelial cells in peripheral blood cells.Intracellular cytokines of inflammatory T-cell subsets were double stained and detected by flow cytometry.Results Under SEM,vascular endothelium in ApoE-/-mice was seriously injured by collagenase Ⅱ with more sites of endothelial erosions compared to normal control group.However,the vascular endothelium from sanchinoside R1 treated mice was slightly damaged with a few sites of endothelial erosions compared to model group.Flow cytometry assay suggested that the proportions of CD62Phi and CD62E+CD62P+ circulating endothelial cells of the model group were significantly increased.Meanwhile,the percentages of TNF-α,IL-17-secreting T lymphocytes were markedly up-regulated along with endothelium injury.After sanchinoside R1 treated,the proportions of CD62Phi and CD62E+CD62P+ circulating endothelial cells were obviously reduced than those of model group,and the percentage of IL-17-secreting T cells was evidently decreased(P<0.05).Conclusions The high percentage of Th17 cells is significantly related to the early process of endothelium disruption.Sanchinoside R1 can selectively down-regulate the proportion of Th17 cells along with a marked protective effect on vascular endothelium lesion.