论文部分内容阅读
目的探讨血管紧张素转化酶抑制剂卡托普利及血管紧张素Ⅱ(AngⅡ)受体拮抗剂氯沙坦对AngⅡ诱导的肿瘤坏死因子-α(TNF-α)、转化生长因子-β1(TGF-β1)表达的干预作用。方法体外原代培养Wistar大鼠主动脉平滑肌细胞,收集不同AngⅡ浓度和作用时间下的细胞和卡托普利组、氯沙坦组和二者联合作用组的细胞,以逆转录(RT)-PCR检测细胞中TNF-α和TGF-β1 mRNA的表达。结果 TNF-αmRNA表达量随AngⅡ浓度和作用时间增加而增加,AngⅡ浓度为10-7、10-6、10-5、10-4 mol/L时表达量分别为(0.43±0.05)、(0.81±0.13)、(0.97±0.17)、(1.09±0.19),与对照组(0.11±0.03)比较,差异有统计学意义(P<0.05或0.01);一定浓度卡托普利(5×10-6mmol/L)、氯沙坦(5×10-6 mmol/L)可明显抑制AngⅡ这一作用;TGF-β1 mRNA表达量随AngⅡ浓度和作用时间增加而明显增加,具有浓度依赖性;在AngⅡ10-7、10-6、10-5和10-4 mol/L时,卡托普利组mRNA表达量分别为(0.19±0.03)、(0.23±0.05)、(0.38±0.14)、(0.34±0.07),较AngⅡ组分别降低了59.57%、73.26%、54.44%和66.67%,差异均有统计学意义(P<0.05或0.01),氯沙坦组分别为(0.17±0.03)、(0.39±0.11)、(0.41±0.12)和(0.39±0.08),较AngⅡ组分别下降了63.82%、54.65%、54.44%和61.76%,差异均有统计学意义(P<0.05)。结论 AngⅡ可促进血管平滑肌细胞TNF-α、TGF-β1 mRNA表达,且有时间和浓度依赖关系;卡托普利、氯沙坦对AngⅡ诱导的血管平滑肌细胞TNF-α、TGF-β1 mRNA表达均有抑制作用,二者联合作用时抑制作用最明显。
Objective To investigate the effects of angiotensin converting enzyme inhibitor captopril and angiotensin Ⅱ receptor antagonist losartan on the expression of tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1) -β1) expression of the intervention. Methods Primary smooth muscle cells of Wistar rats were cultured in vitro and the cells in combination with captopril group, Losartan group and the two groups were collected under different Ang Ⅱ concentration and time. Reverse transcription - PCR was used to detect the expression of TNF-α and TGF-β1 mRNA in the cells. Results The expression of TNF-α mRNA increased with the increase of Ang Ⅱ concentration and duration of action. The expression levels of TNF-α mRNA were (0.43 ± 0.05), (0.81 ± 0.81) and ± 0.13), (0.97 ± 0.17) and (1.09 ± 0.19) respectively, which was significantly different from that of the control group (0.11 ± 0.03) (P <0.05 or 0.01) 6 mmol / L) and Losartan (5 × 10-6 mmol / L) could significantly inhibit the effect of AngⅡ. The expression of TGF-β1 mRNA increased with the increase of AngⅡ concentration and action time in a concentration-dependent manner. (0.19 ± 0.03), (0.23 ± 0.05), (0.38 ± 0.14), (0.34 ± 0.14), respectively in the captopril group at -7, 10-6, 10-5 and 10-4 mol / 0.07), which were significantly lower than that of AngⅡ group by 59.57%, 73.26%, 54.44% and 66.67% respectively (P <0.05 or 0.01), and those in losartan group were (0.17 ± 0.03) and (0.39 ± 0.11), (0.41 ± 0.12) and (0.39 ± 0.08) respectively, which were decreased by 63.82%, 54.65%, 54.44% and 61.76% respectively compared with those in the AngⅡgroup (P <0.05). CONCLUSION: AngⅡ can promote the expression of TNF-α and TGF-β1 mRNA in vascular smooth muscle cells in a time and concentration-dependent manner. Both captopril and losartan can inhibit the expression of TNF-α and TGF-β1 mRNA in vascular smooth muscle cells induced by AngⅡ Have inhibitory effect, the combined effect of inhibition of the two most obvious.