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目的:观察丹皮酚(Pae)对脂多糖(LPS)诱导的大鼠单核细胞(MC)与血管内皮细胞(VEC)黏附功能的影响,研究Pae抗动脉粥样硬化作用的炎症机制。方法:组织块预消化贴壁法分离培养大鼠血管内皮细胞,采用LPS诱导VEC的损伤;健康大鼠灌胃Pae制备含药血清,RP-HPLC法测定血清中Pae含量;MTT法检测Pae对VEC的保护作用;孟加拉玫瑰红染色法检测Pae对LPS诱导的MC与VEC黏附的影响。结果:筛选LPS诱导大鼠MC与VEC黏附的最适浓度为10 ng/mL,作用时间为5 h;以Pae浓度为1.25、2.5、5、10、20μg/mL对损伤的VEC进行干预,当Pae(2.5、5、10μg/mL)作用24 h可有效抑制LPS诱导的MC与VEC的黏附;显著提高LPS导致的VEC存活率的下降。结论:LPS对VEC具有损伤作用,Pae通过提高VEC的存活率,抑制MC与VEC的黏附,以保护VEC免受LPS的损伤。
OBJECTIVE: To observe the effect of pae on the adhesion function of rat monocytes (MC) and vascular endothelial cells (VEC) induced by lipopolysaccharide (LPS), and to study the inflammatory mechanism of Pae against atherosclerosis. Methods: The vascular endothelial cells were isolated and cultured by tissue pre-digestion and adherent method. The injury of VEC was induced by LPS. The serum containing Pae was prepared by intragastric administration of Pae in healthy rats. Pae content was measured by RP-HPLC. VEC. The effect of Pae on adhesion of MC and VEC induced by LPS was detected by Rose Bengal staining. Results: The optimal concentration of LPS-induced MC and VEC adhesion was 10 ng / mL for 5 h. When the Pae concentration was 1.25, 2.5, 5, 10 and 20 μg / mL, Pae (2.5, 5, 10μg / mL) for 24 h effectively inhibited LPS-induced adhesion of MC to VEC and significantly decreased the LVE-induced VEC survival. CONCLUSION: LPS can injure VEC. Pae can inhibit the adhesion of MC and VEC by increasing the survival rate of VEC and protecting VEC from LPS injury.