目的 探讨制何首乌、巴戟天及二者配伍,对氧化型低密度脂蛋白(ox-LDL)诱导的人脐静脉内皮细胞(HUVEC)损伤的影响,以示临床。方法 建立ox-LDL诱导的HUVEC损伤模型,分别用制何首乌、巴戟天、二者配伍的水煮物干预,检测HUVEC的细胞增殖、相对活率、细胞凋亡率、细胞周期、NFκB mRNA的表达。结果 ①制何首乌、巴戟天均能抑制ox-LDL诱导的HUVEC凋亡,二者配伍的抑制作用强于单味中药制何首乌。②制何首乌、巴戟天均能延长ox-LDL诱导的HUVEC的细胞周期(S+G2)%,制何首乌、巴戟天的延长作用相似,二者配伍的延长作用强于单味中药制何首乌、巴戟天。③制何首乌组、巴戟天组的NFκB mRNA的表达量下降,制何首乌组的抑制作用强于巴戟天组,二者配伍的抑制作用强于单味中药制何首乌、巴戟天。结果 制何首乌、巴戟天均能抑制ox-LDL诱导的HUVEC损伤,二者配伍的作用强于单味中药制何首乌、巴戟天。

Objective To investigate the effects of Polygonum multiflorum praeparata, Morinda officinalis and their compatibility on ox-LDL-induced injury of human umbilical vein endothelial cells(HUVEC). Methods We established an ox-LDL-induced HUVEC injury model, made intervention with Polygonum multiflorumpraeparata, Morinda officinalis and their compatibility, the HUVEC cell proliferation, relative viability, apoptosis, cell cycle, NFκB mRNA were detected. Results ①Both Polygonum multiflorumpraeparata, Morinda officinalis reduced the apoptosis rate of HUVEC, and their compatibility had a stronger effect on reducing the apoptosis rate of HUVEC than single Polygonum multiflorumpraeparata. ②Both Polygonum multiflorumpraeparata, Morinda officinalis increased the HUVEC cell cycle (S+G2)%, the extension between Polygonum multiflorumpraeparata and Morinda officinalis was similar, and their compatibility increased HUVEC cell cycle (S+G2)%, it was stronger than single Polygonum multiflorumpraeparata and single Morinda officinalis. ③Both Polygonum multiflorumpraeparata and Morinda officinalis down-regulated the expression of NFκB mRNA in HUVEC, their compatibility down-regulated HUVEC NFκB mRNA expression,it was stronger than Polygonum multiflorumpraeparata, Morinda officinalis. Conclusion Polygonum multiflorumpraeparata, Morinda officinalis and their compatibility can inhibit ox-LDL-induced HUVEC injury, and their compatibility inhibition is stronger than single Polygonum multiflorumpraeparata, and Morinda officinalis.

目的 观察并评估内毒素性急性肺损伤大鼠吸入一氧化氮后外周血中内皮祖细胞和炎症介质的变化情况。方法 90只SPF级健康大鼠分为3组,A组为正常对照组(n=30),B组为急性肺损伤组(ALI)(n=30), C组为一氧化氮(NO)组(n=30)。分别计算各组外周血内皮祖细胞(Endothelial progenitor cells,EPCs) 数量,同时监测肺组织中白细胞介素-10(Interleukin-10,IL-10)水平和髓过氧化物酶(Myeloperoxidase,MPO)活性。结果 我们成功建立了大鼠的ALI肺损伤模型, C组EPCs数量、MPO活性上升幅度均小于B组、而IL-10上升水平均高于B组,差异有统计学意义(P<0.05)。结论 大鼠吸入一氧化氮可减轻内毒素所致急性肺损伤程度,其机制可能与外周血中内皮祖细胞数量及MPO水平下降和IL-10水平上升有关。

Objective To investigate the effect of nitric oxide(NO) inhalation in endotoxin-induced acute lung injury mice. Methods Ninety SPF mice were randomly assigned to the normal group(group A), ALI group(group B)and ALI+NO group(group C). The number of endothelial progenitor cells was counted and the level of Interleukin-10(IL-10) and myeloperoxidase (MPO) were measured. Results Endotoxin administration resulted in pulmonary edema. The pulmonedema was lightened and the level of MPO were decreased by the inhalation of nitric oxide while the level of IL-10 increased. Conclusion NO inhalation can mitigate acute lung injure. The decline of EPCs and MPO and the increase of IL-10 may be one of the mechanism.