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The Regulatory Mechanisms of Bidens philosa on T Helper Cells-Mediated diseases
respiratory airway inflammation
|摘要:||一些文獻指出咸豐草（Bidens pilosa）具有些療效可被用來應用於治療免疫、抗發炎及第二型糖尿病的疾病上，於是我們採取利用以卵清蛋白致敏的動物模式來探討咸豐草在免疫疾病上的作用影響。我們利用醇類（butanol）從咸豐草萃取出來的粗萃取物稱之為BPB （a butanol fraction from B. pilosa），在先前的實驗數據指出BPB可調節輔助型T細胞族群的分化，於是我們建立以ovalbumin (OVA)抗原誘導成氣喘疾病鼠（BALB/c 老鼠）這些動物模式來探討BPB的影響。氣喘發炎現象是由Th2細胞所調節，從動物模式都可觀察到接受BPB處理後其體內由輔助型T細胞分泌的細胞激素其Th2細胞所分泌的IL-4或IL-5有增加的情形，而Th1細胞所分泌的IFN-γ則減少；另外，接受BPB處理的動物體內由Th2細胞調節的免疫球蛋白IgE其表現量也都增加，從粗萃取BPB結果我們得知咸豐草透過影響T細胞族群的分化造成促進Th2調控的免疫疾病。
Bidens pilosa is claimed to be beneficial for immune, anti-inflammatory disorders or diabetes; however, little scientific evidence has been provided concerning its function. We conducted an ovalbumin sensitization animal model to address the immunologic modulation on T cells function of B. pilosa. Preliminary data showed that a butanol fraction (BPB) from B. pilosa can promote the proliferation of naïve helper T cells (Th0) into Th2 but inhibit that of Th0 into Th1. We demonstrated that treatment with BPB deteriorated Th2 cell-mediated respiratory airway inflammation by ovalbumin (OVA) -sensitized BALB/c mice. Th2 cytokines (IL-4 and/or IL-5) increased but Th1 cytokine, IFN-γ, decreased following administration with BPB in BALB/c mice. Accordingly, Th2 cytokine-regulated IgE production in mouse serum was increased with treatment of BPB. We found that BPB had distinct effects on helper T cell-mediated immune disorders possibly via the modulation of T cell differentiation. The BPB could not ameliorate Th2 cell-mediated respiratory airway inflammation, and preliminary data showed that BPB can ameliorated Th1 cell-mediated in non-obese diabetes (NOD) mice . Cytopoliyne(CP), a polyacetylenic glucoside, isolated from BPB, was applied to NOD mice, and the results revealed that CP could protect the β cells from attacking by immune cells. Additionally, it has been reported that polyacetylene in B. pilosa has anti-hyperglycemic activities; and we further investigated the effect of CP on insulin production of β cells. Results revealed that CP could induce the production of insulin in RIN-m5F cells. Taken together, we proposed that B. pilosa could modulate the immunologic responses via the regulation of T helper cell proliferation to change the profiling of cytokine expression, which ameliorated Th1 cell-mediated diabetes was observed in contrast to the enhanced Th2 cell-mediated respiratory airway inflammation. This preventive effect in NOD mice might be not only prevent β-cells from destroying by immune cells but also induce the production of insulin.
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