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目的观察荆芥挥发油(VOHS)对脂多糖(LPS)诱导的急性肺损伤(ALI)大鼠模型肺组织中核因子-κB(NF-κB),IκB-α,IL1-β和TNF-α含量的影响,探讨荆芥挥发油抗炎作用的细胞信号调控转导机制。方法雄性SD大鼠60只随机分为6组,分别为空白对照组,模型对照组,阳性对照组(地塞米松),荆芥挥发油高、中、低剂量组。尾静脉注射LPS(1.0 mg/kg体重)或生理盐水,6h后处死动物,酶联免疫吸附法(ELISA)测定肺组织NF-κB p65、磷酸化IκB-α、IL1-β和TNF-α含量。结果与模型对照组比较,VOHS高、中、低剂量组均可显著降低大鼠肺组织中的NF-κB p65和磷酸化IκB-α含量,差异有统计学意义(P<0.05,P<0.01,P<0.001),同时VOHS各剂量组也可显著降低大鼠肺组织中IL1-β和TNF-α含量,差异有统计学意义(P<0.01,P<0.001)。结论荆芥挥发油抗炎作用机制之一可能是抑制IκB-α磷酸化降解和NF-κB活性,进而减少炎症相关细胞因子IL1-β,TNF-α的合成和释放。
Objective To observe the content of nuclear factor-κB (NF-κB), IκB-α, IL1-β and TNF-α in lung tissue of rat model of acute lung injury (ALI) induced by lipopolysaccharide (LPS) of Schizonepeta volatile oil (VOHS). To investigate the mechanism of cell signal transduction and regulation of anti-inflammatory effects of volatile oil of Schizonepeta. Methods Sixty male Sprague-Dawley rats were randomly divided into 6 groups: blank control group, model control group, positive control group (dexamethasone), and high, medium and low doses of volatile oil of Schizonepeta tenuifolia. LPS (1.0 mg/kg body weight) or normal saline was injected into the tail vein. Six hours later, the animals were killed. The contents of NF-κB p65, phosphorylated IκB-α, IL1-β, and TNF-α in the lung tissue were determined by enzyme-linked immunosorbent assay (ELISA). . Results Compared with the model control group, the VOHS high, middle and low dose groups can significantly reduce the content of NF-κB p65 and phosphorylated IκB-α in rat lung tissue, the difference was statistically significant (P<0.05, P<0.01). (P<0.001). At the same time, VOHS in each dose group also significantly decreased the content of IL1-β and TNF-α in lung tissue of rats, the difference was statistically significant (P<0.01, P<0.001). Conclusion One of the anti-inflammatory mechanisms of the volatile oil from Schizonepeta may be the inhibition of IκB-α phosphorylation and NF-κB activity, which in turn reduces the synthesis and release of inflammatory cytokines IL1-β and TNF-α.