中文摘要：

目的：通过观察痰湿状态下大鼠有机阴离子转运肽oatp2b1基因和蛋白表达来探讨oatp2b1在痰湿转运中的作用。方法：24只大鼠随机分为2组,正常组、模型组各12只。模型组采用高脂饮食造模3个月,每只大鼠取脾、肝、肾组织各1块。采用实时荧光定量PCR、Western Blot方法及免疫组化法检测组织中oatp2b1的基因表达、蛋白表达情况。结果：模型组肝、肾组织中oatp2b1 mRNA表达量高于正常组（P〈0.01,P〈0.05）;而模型组脾组织中oatp2b1 mRNA表达量低于正常组（P〈0.01）。两组oatp2b1蛋白在脾、肝、肾组织有不同程度表达,但差异无统计学意义。模型组中脾脏的巨噬细胞、肝脏的枯否氏细胞及肾小管上皮细胞均有oatp2b1蛋白分布,较正常组表达增强。结论：痰湿伤脾,脾失运化状态下,肝、肾在痰湿转运中发挥重要作用,oatp2b1可能是机体参与痰湿运化的物质基础之一。

英文摘要：

Objective： To explore the effect of organic anion transporting polypeptide （OATP） superfamily member 2bl （oatp2bl） in phlegm-dampness transporting by observing the expression of oatp2bl in gene and protein level in phlegm- dampness rat model. Methods： 24 SD rats were divided randomly into two groups： blank control group and model group. After high fat diet-induced phlegm-dampness rat models were established, the rat were anesthetized, each rat was taken spleen, liver and kidney tissues, and the expression of oatp2bl mRNA and protein were detected in the tissues by fluorescent FQ-PCR, immunohistochemistry （IHC） and western blot techniques. Results： Oatp2bl mRNA and protein were expressed in various degrees. The expression of oatp2bl mRNA in rat liver tissue of model group was up-regulated compared to blank control group （P〈0.01）, the expression of oatp2bl mRNA in rat kidney tissue of model group was up-regulated compared to blank control group （P 〈 0.05）. However, the expression of oatp2blmRNA in rat spleen tissue of model group was down-regulated compared to blank control group （P 〈 0.01）. The oatp2bl protein in spleen, kidney and liver tissues had different degrees of expression, while there was no statistical significance among the two groups by the way of pair-wise comparison. Conclusions： Oatp2bl might be one of the material foundations involved in phlegm-dampness transporting. The changes of expression of oatp2bl mRNA in spleen, kidney and liver tissues suggest that the kidney and liver might play important roles in phlegm-dampness transporting in the state of phlegm-dampness induced by high fat diet.