血胆脂醇过多,它是仔细与胆囊胆汁壅滞有关,由增加 Oddi 的括约肌的紧张的 Oddi 机能障碍(草皮) 的罐头原因括约肌(那么) 。细胞内部的钙离子集中([Ca~(2+)] _i )能影响敏感K~+隧道(BK_( Ca ))能提高的大传导力的Ca~(2+)的 SO.Thebeta1 子单元的紧张BK_( Ca )隧道到的敏感[Ca~(2+)],BK_( Ca )隧道 subunitbeta1 的缺席和衰落能导致许多疾病。然而,在血胆脂醇过多之间的关系和 beta1 子单元的表示很好没被理解。在这研究,我们成功地表示了并且净化兔子BK_( Ca ) beta1 子单元蛋白质并且准备了它准备抗体的 polyclonal antibody.Thespecificity 被草皮兔子模型由一本高胆固醇食谱导致了的西方的 blotting.A 决定被建立并且 beta1 子单元的表示被免疫那么决定组织化学的染色并且西方弄污。与控制相比,我们的结果证明血胆脂醇过多能减少 beta1 子单元在的表示那么从兔子的房间。这显示 BK_(Ca ) 隧道 beta1 子单元的那更低的表情可能导致草皮。
Hypercholesterolemia, which is closely related to gallbladder bile stasis, can cause sphincter of Oddi dysfunction (SOD) by increasing the tension of sphincter of Oddi (SO). Intracellular calcium ion concentration ([Ca2+]i) could influence the tension of SO. The β1 subunit of the big-conductance Ca^2+ sensitive K+ channel (BKCa) can enhance the sensitivity of the BKCa channel to [Ca2+]i. Absence and decline of the BKca channel subunit β1 could lead to many diseases. However, the relationship between hypercholesterolemia and the expression of β1 subunit is not well understood. In this study, we successfully expressed and purified the rabbit BKca β1 subunit protein and prepared its polyclonal antibody. The specificity of the prepared antibody was determined by western blotting. A SOD rabbit model induced by a high cholesterol diet was established and the expression of the β1 subunit of SO was determined by immunohistochemical staining and western blotting. Compared with the controls, our results demonstrated that hypercholesterolemia could decrease the expression of the β1 subunit in the SO ceils from rabbits. This indicates that lower expression of BKca channel β1 subunit might induce SOD.