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目的探讨血清抗β1肾上腺素能和M2胆碱能受体自身抗体是否与糖尿病大鼠肾损害有关。方法以链脲佐霉素(STZ)诱导的糖尿病大鼠(DM组)作为研究对象,以正常Wistar大鼠(健康对照组)作为对照。以合成的β1-受体(β1-R)和M2-受体(M2-R)多肽片段为抗原,应用酶联免疫吸附测定(ELISA)技术,检测各组大鼠血清中抗β1-R和M2-R自身抗体,计算阳性率,并以血清自身抗体的测定结果,将DM组进一步分为抗β1-R、M2-R抗体均阴性组(抗体阴性组),仅抗β1-R抗体阳性组(β1组),仅抗M2-R抗体阳性组(M2组),抗β1-R、M2-R抗体均阳性组(β1+M2组));观测大鼠体重、肾重及肾脏肥大指标(肾重/体重);用放射免疫法测尿微量白蛋白和尿α1微球蛋白。结果健康对照组中,抗β1-R抗体阳性、抗M2-R抗体阳性各1只(阳性率均为10%);糖尿病大鼠中,抗β1-R和M2-R抗体阳性率分别为46.67%、53.33%,其中抗β1-R和M2-R抗体同时存在的阳性率为30.0%。各组大鼠肾重无明显差异(P>0.05),β1+M2组的体重明显低于抗体阴性组、β1组、M2组(P<0.05)和健康对照组(P<0.01),肾重/体重比值、尿微量白蛋白和尿α1微球蛋白明显高于抗体阴性组、β1组、M2组(P<0.05)和健康对照组(P<0.01)。结论抗β1-R和M2-R自身抗体的产生可能与糖尿病鼠肾损害有关。发生机制有待进一步探讨。
Objective To investigate whether serum anti-β1 adrenergic and M2 cholinergic autoantibodies are associated with renal damage in diabetic rats. Methods Streptozotocin (STZ) -induced diabetic rats (DM group) were used as research objects, and normal Wistar rats (healthy control group) as control. The anti-β1-R and M2-R fragments of anti-β1-R and M2-R fragments were detected by enzyme linked immunosorbent assay (ELISA) M2-R autoantibodies to calculate the positive rate, and the results of serum autoantibodies, the DM group is further divided into anti-β1-R, M2-R antibody negative group (antibody negative group), only anti-β1-R antibody positive (Β1 group), M2 group (M2 group), anti-β1-R group and M2-R group (β1 + M2 group). The body weight, kidney weight and renal hypertrophy index (Kidney weight / body weight); urine microalbuminuria and urine α1 microglobulin were measured by radioimmunoassay. Results The positive rate of anti-β1-R and anti-M2-R was 1% (positive rate was 10%) in healthy controls. The positive rates of anti-β1-R and M2-R in diabetic rats were 46.67 % And 53.33%, respectively. The positive rate of coexistence of anti-β1-R and M2-R antibodies was 30.0%. The body weight of β1 + M2 group was significantly lower than that of antibody negative group, β1 group, M2 group (P <0.05) and healthy control group (P <0.01), kidney weight / Body weight ratio, urine microalbuminuria and urinary α1 microglobulin were significantly higher than those in antibody negative group, β1 group, M2 group (P <0.05) and healthy control group (P <0.01). Conclusion The production of anti-β1-R and M2-R autoantibodies may be related to renal damage in diabetic rats. The mechanism needs to be further explored.