亚急性瘤胃酸中毒(SARA)是育肥牛羊常见多发疾病，其特征是瘤胃短链脂肪酸(SCFA)蓄积。SCFA蓄积的主要原因是生成增加和吸收障碍，目前还不清楚瘤胃SCFA吸收障碍的原因和机制。SLC22A作为有机阴离子转运蛋白在瘤胃上皮SCFA吸收过程中发挥重要作用，而在瘤胃SCFA蓄积形成的低pH状态下，有可能改变瘤胃上皮SLC22A介导的SCFA吸收模式。本项目拟通过诱发绵羊SARA在体实验和模拟SARA体外实验，观测SLC22A家族成员在瘤胃上皮的表达、分布和细胞定位；观测HCO3-对瘤胃上皮SLC22A介导的SCFA转运的影响，证实SLC22A介导的SCFA转运是否依赖HCO3-；观测SCFA蓄积对瘤胃上皮SLC22A家族成员表达的影响及其与SCFA吸收的关系，确认瘤胃pH降低可干扰SLC22A介导的SCFA转运。为揭示SLC22A在SARA所致的瘤胃SCFA蓄积中的作用提供理论基础。

Subacute ruminal acidosis (SARA), is a common disease for fattening cattle and sheep, is characterized by short chain fatty acids (SCFA) accumulation in the rumen.Ruminal SCFA accumulation was resulted from SCFA excess production and malabsorption. However, the few studies was fcuosed on the molecule mechanism of SCFA malabsorption. SLC22A, an organic anion transport protein, plays an important role in the uptake of SCFA in the ruminal epithelium cell. SCFA accumulation could induce low pH, which may infulence with the uptake of SCFA medicated by SLC22A. In this study, sheep with SARA and ruminal epithelium cell cultured in vitro were used. The expressions,distribution,and cellular localization of SLC22A in the ruminal epithelium were detected.The effects of HCO3- on the SCFA transport medicated by SLC22A were determinated, which revealed HCO3- could infulence with the SCFA transport through SLC22A. The effects of SCFA accumulation on the expression of SLC22A and SCFA uptake in the ruminal epithelium were detected, which indicated that low pH affected the SCFA transport medicated by SLC22A. This study will provide valuable information to understand the role of SLC22A in the SCFA accumulation induced by SARA.