Captopril-induced reduction of serum levels of transforming growth factor-beta1 correlates with long-term renoprotection in insulin-dependent diabetic patients.
Captopril-induced reduction of serum levels of transforming growth factor-beta1 correlates with long-term renoprotection in insulin-dependent diabetic patients.
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卡托普利诱导的转化生长因子-β1 血清水平降低与胰岛素依赖型糖尿病患者的长期肾脏保护作用相关。
DOI：
10.1016/s0272-6386(99)70037-5
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Lewis,EJ
中科院分区：
文献类型：
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作者：
Sharma,K;Eltayeb,BO;McGowan,TA;Dunn,SR;Alzahabi,B;Rohde,R;Ziyadeh,FN;Lewis,EJ
合作研究小组Captopril试验证实了Captopril对糖尿病肾病进展的肾保护作用，并且可能不依赖于血压。由于已知血管紧张素II可刺激促肾上腺皮质激素细胞因子转化生长因子-β（TGF-β），我们推测肾保护作用可能是由于抑制TGF-β1的产生。在卡托普利试验中，在基线和6个月时测量血清中的TGF-β1水平。对所有可用的患者血清进行TGF-β1分析。对前6个月内TGF-β1水平的百分比变化与随后2年内肾小球滤过率（GFR）的百分比变化进行分析。安慰剂组（n = 24）TGF-β1水平升高11%（P = 0.003），而卡托普利组（n = 34）TGF-β1水平降低14%（P = 0.01）。在安慰剂组（r =-0.55，P = 0.005）和卡托普利组（r =-0.45，P = 0.008）患者中，前6个月内TGF-β1水平的百分比变化与随后2年内GFR的百分比变化之间呈负相关。在初始GFR低于75 mL/min的患者中，安慰剂组（n = 9，r =-0.69，P = 0.03）和卡托普利组（n = 21，r =-0.73，P = 0.0001）的TGF-β1水平变化百分比与GFR变化百分比之间的相关性更强。我们的数据表明，卡托普利降低糖尿病肾病中TGF-β1水平，TGF-β1水平的变化可能预测糖尿病肾病的病程。
The renoprotective effect of captopril on progression of diabetic nephropathy was demonstrated by the Collaborative Study Group Captopril Trial and might be independent of blood pressure. Because angiotensin II is known to stimulate the prosclerotic cytokine, transforming growth factor-β (TGF-β), we postulated that the renoprotective effect may be due to inhibition of TGF-β1 production. TGF-β1 levels were measured in serum at baseline and 6 months from patients in the captopril trial. TGF-β1 analyses were performed on all available patient sera. Analysis was performed between the percent change in TGF-β1 levels during the first 6 months versus the percent change in glomerular filtration rate (GFR) in the subsequent 2 years. TGF-β1 levels increased by 11% (P = 0.003) in the placebo group (n = 24), whereas there was a decrease of 14% (P = 0.01) in the captopril group (n = 34). There was an inverse correlation between the percent change in TGF-β1 levels during the first 6 months and the percent change in GFR over the ensuing 2-year period in patients from both the placebo (r = −0.55, P = 0.005) and captopril groups (r = −0.45, P = 0.008). In patients with initial GFR below 75 mL/min, there was an even stronger correlation in percent change in TGF-β1 levels and percent change in GFR in both placebo (n = 9, r = −0.69, P = 0.03) and captopril groups (n = 21, r = −0.73, P = 0.0001). Our data suggest that captopril decreases TGF-β1 levels in diabetic nephropathy and that changes in TGF-β1 levels may predict the course of diabetic nephropathy.