脂多糖对肺微血管内皮细胞β-受体及β-受体激酶影响的研究  

EFFECTS OF LIPOPOLYSACCHARIDE ON β-ADRENOCEPTOR AND β-ADRENOCEPTOR KINASES IN RAT PULMONARY MICROVASCULAR ENDOTHELIAL CELLS

作　　者：肖贞良[1] 钱桂生[1] 孙耕耘[2] 夏前明[1] 

机构地区：[1]第三军医大学新桥医院全军呼吸病研究所 [2]安徽医科大学附属医院

出　　处：《解放军医学杂志》2003年第2期119-121,共3页Medical Journal of Chinese People's Liberation Army

基　　金：国家自然科学基金资助课题 (编号 30 0 70 334 ;39730 2 1 0 )

摘　　要：为探讨脂多糖 (LPS)对肺微血管内皮细胞 β 受体 (β AR)及 β AR激酶的影响 ,在体外分离、培养大鼠肺微血管内皮细胞(RPMVEC)的基础上 ,采用放射性配基结合法检测LPS作用后RPMVECβ AR的变化 ,并用Westernblot检测了LPS作用后 β AR激酶GRK2和GRK3的改变。结果发现 ,β AR最大结合容量BmaxLPS组显著低于正常对照组(P <0 0 5 ) ,LPS+山莨菪碱组与正常对照组间无显著性差异 ;LPS组与LPS+山莨菪碱组间GRK2表达无明显差异 ,但均明显高于正常对照组 ;RPMVEC无GRK3表达。提示LPS作用后引起的RPMVECβ AR下调可能与GRK2表达增加促进了β AR内化有关 ,而与GRK3无关 ;山莨菪碱不是通过抑制GRK2表达而是通过其他机制抑制LPS引起的βIn order to probe the effects of lipopolysaccharide(LPS) on β adrenoceptor (β AR) and β AR kinases in rat pulmonary microvascular endothelial cells (RPMVEC), radioactive ligand binding assay was used to measure the distribution density of β AR before and after LPS acting in it; Western blot was used to observe the expression changes in β AR kinases, including GRK2 and GRK3. The results showed that the maximum binding capacity (Bmax) of RPMVEC β AR was 5 583±0 306 fmol/10 5 cells. The Bmax of β AR in LPS group significantly decreased compared with normal control group ( P <0 05) and no significant difference was found between normal control group and LPS+anisodamine group. The expression of GRK2 in LPS group and LPS+anisodamine group increased obviously compared with normal control group and no GRK3 expression was found in RPMVEC. The results suggest that the increased expression of GRK2 but not GRK3 induced by LPS in RPMVEC may promote the internalization of β AR, which further leads to the down regulation of β AR. Anisodamine may inhibit the down regulation of β AR through other mechanism instead of inhibiting the expression of GRK2.

关 键 词：肾上腺素能Β受体 G蛋白偶联受体激酶 肺微血管内皮细胞 大鼠 脂多糖类 肺疾病 

分 类 号：R563.02[医药卫生—呼吸系统] R363[医药卫生—内科学]