人参单体皂甙Rh2对非小细胞肺癌患者肺泡巨噬细胞免疫活性的影响

目的:探讨人参单体皂甙Rh2(G-Rh2)对非小细胞肺癌患者肺泡巨噬细胞(AM)分泌细胞毒效应分子的影响.方法:采用ELISA法和酶法分别检测35例非小细胞肺癌患者支气管肺泡灌洗液及其AM培养上清液中肿瘤坏死因子(TNF-α)和NO浓度,并分别用干扰素-α(IFN-α)、G-Rh2以及两药联合干预AM培养,检测其上清液中TNF-α和NO变化情况.结果:所有非小细胞肺癌患者其AM均可产生一定量的TNF-α和NO;非小细胞肺癌患者荷瘤侧肺NO和TNF-α活性在肺泡灌洗液及AM培养上清液中均明显低于非荷瘤侧肺.G-Rh2干预下AM培养上清液中TNF-α和NO的浓度较对照组明显升高(P＜0.05);与TNF-α干预AM培养上清液中TNF-α和NO的浓度比较差异无统计学意义(P＞0.05).G-Rh2和TNF-α联合干预时AM培养上清液中TNF-α和NO的浓度明显大于TNF-α或G-Rh2单独干预(P＜0.01).结论:G-Rh2能促进非小细胞肺癌患者肺泡巨噬细胞分泌细胞毒效应分子,联合干扰素时其作用更显著,两者具有协同性.

Effect of ginsenoside Rh2 on immunocompetence of alveolarmacrophages in patients with non-small cell lung cancer

OBJECTIVE: To explore the effect of ginsenoside Rh2(G-Rh2) on the excretion of cytotoxin-effecting molecule of alveolar macrophages(AM) in patients with non-small cell lung cancer(NSCLC). METHODS: The concentration of tumor necrosis factor(TNF-alpha) and NO in the bronchoalveolar lavage fluid(BALF) and the cultured supernatants of AM in 35 patients with NSCLC were measured by ELISA and enzyme method,and levels of TNF-alpha and NO in the cultured supernatants of AM after being cultivated with IFN-alpha,G-Rh2,and IFN-alpha+G-Rh2 were measured by the same method. RESULTS: AM in all the non-small cell lung cancer patients produced TNF-alpha and NO.The activity of TNF-alpha and NO was lower in the BALF and in the cultured supernatants of AM of the tumor-bearing lungs than that of the non-tumor-bearing lungs.The concentrations of TNF-alpha and NO in the cultured supernatants of AM cultivated with G-Rh2 were higher than those in the control (P<0.05),but there were no significant differences between the G-Rh2 group and IFN-alpha group (P>0.05). The concentrations of TNF-alpha and NO in the cultured supernatants of AM cultivated with both G-Rh2 and IFNalpha were obviously higher than those stimulated with IFNalpha or G-Rh2 (P<0.01) alone. CONCLUSION: G-Rh2 can enhance the excretion of cytotoxin-effecting molecules of AM in patients with NSCLC. The changes are more distinctive when G-Rh2 and IFNalpha have coordinated action.