论文部分内容阅读
为探讨烫伤引起病理性应激时大鼠肾胞液醛固酮结合活性的变化及可能的调节机制 ,以 [3H] 醛固酮为配体 ,用放射性配基 受体结合分析法测定了正常对照组、轻度烫伤组和重度烫伤组大鼠肾胞液醛固酮结合活性的结合容量 (Rt)和表观解离常数 (Kd) ;采用体内注射TNF α、IL 1β中和抗体和α 促黑色素细胞刺激激素 (α melanocyte stimulatinghormone,α MSH)和合成肽KPV (Ac D Lys L Pro D Val)等措施调节其改变。结果发现 ,肾胞液存在两种不同结合容量、不同亲和力的醛固酮结合活性受体。与正常对照组的Rt (Rt1:4 1 6± 7 2fmol/mgpro ;Rt2 :3 17 6± 70 0fmol/mgpro)相比 ,轻烫组的Rt(Rt1:4 1 4± 5 0fmol/mgpro ;Rt2 :3 14 8± 4 5 7fmol/mgpro)无显著差异 (P >0 0 5 ;P >0 0 5 ) ;重烫组的Rt(Rt1:2 2 4± 5 4fmol/mgpro ;Rt2 :196 3± 3 2 5fmol/mgpro)则显著下降(P <0 0 1;P <0 0 1)。体内注射TNF α与IL 1β中和抗体、α MSH及KPV均能明显提高重烫组Rt值。结果提示 ,重度烫伤大鼠肾胞浆醛固酮结合活性降低 ,TNF α、IL 1β中和抗体、α MSH及KPV均可防止重度烫伤引起病理性应激时醛固酮结合活性降低。
To investigate the changes of aldosterone-binding activity in renal cytoplasm of rats induced by scald and its possible regulatory mechanism, the [3H] aldosterone was used as a ligand and the radioactive ligand receptor binding assay was used to determine the changes of aldosterone-binding activity, (Rt) and apparent dissociation constant (Kd) of renal aldosterone-binding activity in rats with severe scald and severe scald. The effects of injecting TNFα, IL-1β neutralizing antibody and α-melanocyte stimulating hormone ( α melanocyte stimulating hormone, α MSH) and synthetic peptide KPV (Ac D Lys L Pro D Val). As a result, it was found that there are two different receptors of aldosterone binding activity in renal cell solution that have different binding capacities and different affinities. Compared with the normal control group, Rt (Rt1: 4 1 4 ± 5 0 fmol / mgpro; Rt2: 3 17 6 ± 70 0 fmol / mgpro) : 3 14 8 ± 4 5 7fmol / mgpro) had no significant difference (P> 0 05; P 0 05). The Rt (1 2 4 ± 5 4fmol / mgpro; Rt 2: 196 3 ± 3 2 5fmol / mgpro) decreased significantly (P <0.01; P <0.01). In vivo injection of TNFα and IL 1β neutralizing antibodies, α MSH and KPV can significantly improve the scalded group Rt value. The results suggest that the aldosterone binding activity of renal cytoplasm in severely scalded rats is decreased, neutralizing antibodies TNF α, IL 1β, α MSH and KPV can prevent the decrease of aldosterone binding activity in pathological stress caused by severe scald.