芜菁中性多糖对A549荷瘤小鼠免疫功能的影响

Effects of neutral polysaccharide from Brassica rapa L. on immune function of A549 tumor-bearing mice

中文关键词:  芜菁  中性多糖  A549细胞  荷瘤小鼠

英文关键词:Brassica rapa L.  neutral polysaccharide  A549 cells  tumor-bearing mice

中文摘要:

      目的 探究芜菁中性多糖对A549小鼠移植瘤模型肿瘤微环境及凋亡相关蛋白、细胞因子水平的影响。方法 实验采用酶联免疫法、HE染色法、免疫组化法, 检测半胱氨酸天冬氨酸蛋白酶3 (cysteinyl aspartate specific proteinase 3, caspase-3)、白细胞介素2 (interleukin-2, IL-2)、白细胞介素6 (interleukin-6, IL-6)、白细胞介素12 (interleukin-12, IL-12)和肿瘤坏死因子-α (tumor necrosis factor-α, TNF-α)含量及B淋巴细胞瘤-2 (B-cell lymphoma-2, Bcl-2)、Bcl-2相关X蛋白(Bcl-2 associated X protein, Bax)相对表达水平, 计算免疫器官指数、抑瘤率。结果 芜菁中性多糖中、高剂量组能使A549荷瘤小鼠肿瘤组织caspase-3蛋白含量显著增加(P<0.01); 使小鼠血清中IL-2、IL-6、IL-12、TNF-α含量升高(P<0.01); Bcl-2蛋白表达水平降低, Bax蛋白表达水平升高(P<0.01)。结论 芜菁中性多糖对人肺腺癌细胞A549生长具有抑制作用, 可提高A549荷瘤小鼠的脾脏指数和胸腺指数, 下调Bcl-2蛋白, 上调Bax蛋白的表达, 减轻荷瘤小鼠脏器病理损伤。

英文摘要:

      Objective To study the effects of Brassica rapa L. neutral polysaccharide on apoptosis-related polypeptide and cytokines of transplanted mice model of A549 carcinoma in vitro. Methods Enzyme-linked immunosorbent assay, HE staining and immunohistochemistry were used to detect cysteinyl aspartate specific proteinase 3 (caspase-3), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-12 (IL-12), and tumor necrosis factor-α (TNF-α) content and B-cell lymphoma-2 (Bcl-2), the relative expression level of Bcl-2 associated X protein (Bax), and the immune organ index and tumor inhibition rate were calculated. Results The moderate and high dose groups of Brassica rapa L. neutral polysaccharide could significantly increase the caspase-3 protein content in A549 tumor-bearing mice (P<0.01). The content of IL-2, IL-6, IL-12 and TNF-α in serum of mice were increased (P<0.01). The expression level of Bcl-2 protein was decreased, while that of Bax protein was increased (P<0.01). Conclusion Brassica rapa L. neutral polysaccharides can inhibit growth of A549 human lung adenocarcinoma cells, increase the spleen index and thymus index of A549 tumor-bearing mice, increase the expression of Bax protein through downregulation of Bcl-2 protein, and reduce the pathological damage in tumor-bearing mice.