| 高月求,孙学华,章晓鹰,王灵台.补肾方对慢性乙型肝炎T细胞亚群及其功能的影响[J].,2005,(5):408-411 |
| 补肾方对慢性乙型肝炎T细胞亚群及其功能的影响 |
| Effect of Bushen Recipe on T-cell Subsets and Their Function in Patients with Chronic Hepatitis B |
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| DOI： |
| 中文关键词: 慢性乙型肝炎 T细胞 补肾方 |
| 英文关键词:chronic hepatitis B T-cell Bushen recipe |
| 基金项目:上海市教委课题(No.303041809) |
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| 中文摘要: |
| 目的观察补肾方对慢性乙型肝炎患者免疫功能状态的调节作用。方法收集HBeAg阳性ALT异常者30例,给予补肾方治疗,用药6个月,于用药前、用药3个月、6个月时分别检测下列指标。采用罗氏荧光定量PCR法检测HBVDNA ,外周血单个核细胞(peripheralbloodmononuclearcell,PBMC)加入HBeAg、HBcAg与植物血凝素(Phytohemagglutinin ,PHA)培养48h ,检测培养上清液中IL 10、IFN -γ,血液中CD4+、CD8+、CD8+CD2 8+、CD8+CD2 8-和CD2 8+T细胞的比例及加入HBeAg、HBcAg与PHA培养48h后培养细胞中CD8+CD2 8+的比例。结果补肾方治疗有效组在治疗3个月后,PBMC培养中IFN- γ较治疗前明显上升,IL- 10明显下降(P <0 . 0 5,P <0. 0 1) ;CD8+CD2 8+T、CD2 8+T、培养后CD8+CD2 8+T细胞较治疗前明显上升,CD8+CD2 8-T细胞明显下降(P <0 .0 5或P <0 .0 1)。结论补肾方能明显增强Th1型细胞因子的表达,降低Th2型细胞因子的表达,促进CD8+(CytotoxicTlymphocyte ,CTL)的表达,这可能是使HBVDNA复制得到抑制的机制之一。 |
| 英文摘要: |
| ObjectiveTo observe the regulatory effect of Bushen recipe （BSR） on immune function in patients with chronic hepatitis B. MethodsThirty patients with HBeAg +and abnormal alanine transaminase （ALT） level were treated with BSR for 6 months. The following parameters before treatment, 3 months and 6 months after treatment were tested: （1） HBV DNA by fluorescence quanitiative PCR; （2） Levels of interleukin-10 （IL-10） and interferon-γ in supernatant of cultured peripheral blood mononuclear cell （PBMC） after had been cultured with HBeAg, HBcAg and phytohemagglutinin （PHA） for 48 hrs; （3） Blood levels of T-cells, including CD4 +,CD8 +, CD8 +CD 28 +, CD8 +CD 28 - and CD 28 +, and their ratio, as well as the percentage of CD8 +CD 28 + in the cell culture after being co-cultured with PHA for 48 hrs. ResultsIn patients effectively treated by BSR, after 3 months treatment, level of IFN-γ in PBMC culture significantly increased, CD8 +CD 28 +, CD 28 + T-cells significantly enhanced and IL-10 and CD8 +CD 28 + T-cells significantly decreased （P<0.05, P<0.01）. ConclusionBSR could significantly strengthen the expression of Th1 type cytokine, decrease the expression of Th2 type cytokine and promote the expression of CD8 + cytotoxic T-lymphocyte, which may be one of mechanisms in suppressing HBV DNA replication. |
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