目的研究过度表达人C-反应蛋白(hCRP)对大鼠血压的影响及其相关机制。方法以重组腺相关病毒为载体,介导hCRP基因(CRP组)或对照基因(GFP组)在大鼠体内表达,观察实验动物血压变化,并以western blot方法检测大鼠主动脉血管紧张素1型受体(AT_1),血管紧张素2型受体(AT_2)的表达。结果CRP组大鼠血压从基因注射后2月开始升高,升高血压的效应在基因导入3月后保持稳定(与对照组相比约升高21 mm Hg)并持续到实验结束。而GFP组血压无明显变化。Western blot结果显示,与对照组相比,CRP组大鼠主动脉AT_1蛋白水平升高,而AT_2蛋白水平降低。结论重组腺相关病毒介导的hCRP过表达可以导致大鼠血压升高,其机制与增加主动脉AT_1表达,降低AT_2表达有关。
Increased plasma total homocysteine (tHcy) and high sensitivity C-reactive protein (hsCRP) levels are independent risk factors for cardiovascular disease.However, the predictive value of tHcy in combination with hsCRP in patients with stroke is not known.To determine the relationship between tHcy and hsCRP, we enrolled 291 patients with first-onset stroke (196 ischemic and 95 hemorrhagic).Plasma tHcy and hsCRP levels were measured and subsequent vascular events and deaths were determined over a 5-year period.Using the arbitrary cutoff for tHcy (<18 μmol/L and ≥18 μmol/L) and hsCRP (<1 mg/L, 1-3 mg/L and >3 mg/L), the patients were divided into 6 groups.Survival analysis showed that the probability of death or new vascular events during a 5-year follow-up increased according to tHcy and hsCRP levels (P<0.01).The relative risk (RR) of death or new vascular events was 4.67 (95% CI, 1.96 to 11.14, P=0.001) in patients with high tHcy (≥18 μmol/L) and hsCRP (>3 mg/L) compared with those with low tHcy (<18 μmol/L) and hsCRP (<1 mg/L).The increased tHcy level (≥18 μmol/L) combined with increased hsCRP level (>3 mg/L) was still significantly associated with the risk of death or new vascular events (RR, 4.10, 95% CI, 1.61 to 10.45, P=0.003) even when adjusted for other risk factors at inclusion.The combination of increased tHcy and hsCRP levels had a stronger predictive value than increased hsCRP alone or increased tHcy level alone.Further studies are required to evaluate the potential decrease in risks associated with lowering both Hcy and hsCRP levels in patients that present with both increased tHcy and hsCRP.
