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目的观察中药粉防己碱对高脂饮食兔血清白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)及血管壁细胞核因子-κB表达的影响,进一步探讨粉防己碱抗动脉粥样硬化的机制。方法将18只雄性日本大耳白兔随机分为正常对照组(普通饲料)、高脂模型组(高脂饲料)和粉防己碱组(高脂饲料+粉防己碱)。喂养12周后处死动物,放射免疫法检测血清IL-1β,TNF-α含量;采用逆转录聚合酶链式反应对血管壁细胞核因子-κBmRNA表达定量分析;Western杂交定量分析血管壁细胞核因子-κBp65蛋白亚基。结果高脂模型组血清IL-1β,TNF-α显著高于正常对照组和粉防己碱组(P<0.05),正常对照组和粉防己碱组差异无显著性意义(P>0.05);高脂模型组(1.414±0.106)NF-κBmRNA显著高于正常对照组(0.085±0.062)和粉防己碱组(0.453±0.034),而高脂模型组NF-κB蛋白亚基p65(10.08±5.75)显著低于正常对照组(35.90±3.07)和粉防己碱组(35.91±4.38)(P<0.001)。结论粉防己碱有抑制炎症因子IL-1β,TNF-α合成和分泌的作用;高血脂激活NF-κB,p65易位入胞核促进转录而降解,而粉防己碱对其有抑制作用,这可能是粉防己碱抗AS作用的机制。
Objective To observe the effects of tetrandrine, a traditional Chinese medicine, on serum interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and vascular wall cell nuclear factor-κB expression in high-fat diet rabbits, and further explore the anti-tetrandrine resistance Atherosclerosis mechanism. Methods 18 male Japanese white rabbits were randomly divided into normal control group (normal diet), high-fat model group (high-fat diet) and tetrandrine group (high-fat diet + tetrandrine). After 12 weeks of feeding, animals were sacrificed. The levels of serum IL-1β and TNF-α were determined by radioimmunoassay. The expression of NF-κB mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). Western-blot quantitative analysis of vascular wall cells nuclear factor-κBp65 Protein subunits. Results The levels of serum IL-1β and TNF-α in the high-fat model group were significantly higher than those in the normal control group and tetrandrine group (P<0.05). There was no significant difference between the normal control group and tetrandrine (P>0.05). The level of NF-κB mRNA in the lipid model group (1.414±0.106) was significantly higher than that in the normal control group (0.085±0.062) and tetrandrine group (0.453±0.034), while the NF-κB protein subunit p65 in the high-lipid model group (10.08±5.75). Significantly lower than the normal control group (35.90±3.07) and tetrandrine group (35.91±4.38) (P<0.001). Conclusion Tetrandrine can inhibit the synthesis and secretion of inflammatory cytokines IL-1β and TNF-α. Hyperlipidemia activates NF-κB, and p65 translocates into nucleus to promote transcription and degradation, while tetrandrine has inhibitory effect on it. It may be the mechanism of anti-AS action of tetrandrine.