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目的 :探讨血管紧张素Ⅱ (AngⅡ )对近端肾小管上皮细胞DNA、RNA及蛋白质合成的作用。 方法 :采用3H标记的胸腺嘧啶核苷 (3HT)、3H标记的尿嘧啶核苷 (3HU)及3H标记的脯氨酸 (3HP)掺入的方法 ,观察AngⅡ对无血清培养的LLC PK1细胞DNA、RNA及蛋白质合成的作用。 结果 :AngⅡ刺激 2 4、48和 72h ,LLC PK1细胞3HT掺入与对照组相比无明显变化。AngⅡ刺激 48h ,3HU掺入的min-1值明显升高 (4 2 42± 6 6 9、4119± 5 71及3 972± 5 6 4vs 3 2 2 0± 2 6 5 ,10 -10 、10 -8及 10 -6mol/LvsControl,P <0 0 5 ) ;同样 ,3HP掺入的min-1值也有明显升高(6 2 0 72± 10 912、6 3 736± 92 11及 6 45 0 7± 15 5 90vs 492 40± 70 45 ,10 -10 、10 -8、及 10 -6mol/LvsControl,P <0 0 5 )。缬沙坦 (10 6mol/L)可以阻断AngⅡ刺激LLC PK13HU及3HP掺入的作用。 结论 :①AngⅡ可以刺激LLC PK1细胞RNA及蛋白质合成 ,而对LLC PK1细胞DNA合成无明显促进作用 ,表明AngⅡ可以诱导LLC PK1细胞肥大而不是增生。②血管紧张素Ⅱ 1型受体拮抗剂对AngⅡ诱导的LLC PK1细胞肥大有明显抑制作用。
Objective: To investigate the effect of angiotensin Ⅱ on DNA, RNA and protein synthesis in proximal renal tubular epithelial cells. Methods: 3H-labeled 3H-thymidine (3HT), 3H-labeled uridine (3HU) and 3H-labeled proline (3HP) were used to detect the effect of AngⅡ on LLC PK1 cell DNA , RNA and protein synthesis. Results: 3HT incorporation of LLC PK1 cells at 2, 48 and 72 h after AngⅡ stimulation did not change significantly compared with the control group. After stimulated with AngⅡ for 48h, the 3H-incorporation of min-1 was significantly increased (4242 ± 6 6, 4191 ± 5 71 and 3972 ± 564 vs 3220 ± 2 6 5, 10 -10, 8 and 10 -6 mol / L vs Control, P <0 05). Likewise, min-1 values of 3HP incorporation were also significantly increased (6 2 0 72 ± 10 912, 6 3 736 ± 92 11 and 6 45 0 7 ± 15 5 90 vs 492 40 ± 70 45, 10 -10, 10 -8, and 10 -6 mol / L vs Control, P <0 0 5). Valsartan (10 6mol / L) could block the effect of AngⅡ-stimulated LLC PK13HU and 3HP incorporation. Conclusion AngⅡ can stimulate the RNA and protein synthesis of LLC PK1 cells, but not significantly promote the DNA synthesis of LLC PK1 cells, indicating that Ang Ⅱ can induce LLC PK1 cells to hypertrophy rather than hyperplasia. ② angiotensin Ⅱ type 1 receptor antagonist Ang Ⅱ induced LLC PK1 cell hypertrophy significantly inhibited.