Mirjanic-Azaric Bosa, Rizzo Manfredi, Jürgens Günther, Hallstroem Seth, Srdic Svetozar, Marc Janja, Cerne Darko
Clinical Centre Banja Luka , Banja Luka , Bosnia and Herzegovina.
Scand J Clin Lab Invest. 2015 Sep;75(5):382-9. doi: 10.3109/00365513.2015.1031691. Epub 2015 Apr 29.
In vitro and animal studies indicate that statins increase heme oxygenase-1 gene (HMOX1) expression, which then, presumably, increases plasma bilirubin concentration. However, clinical confirmation that statins concomitantly increase HMOX1 expression and plasma bilirubin concentration is lacking. We hypothesized that in patients with stable angina atorvastatin therapy (20 mg/day for 10 weeks) concomitantly increases total bilirubin concentration and HMOX1 expression, as assessed non-invasively by plasma analysis.
In 44 patients with stable angina plasma concentrations of total bilirubin, HMOX1 mRNA and HMOX1 protein were measured before and after the statin treatment, as well as plasma concentrations of oxidized low-density lipoprotein (OxLDL), malondialdehyde (MDA), monocyte chemoattractant protein (MCP-1) and C-reactive protein (CRP).
Atorvastatin treatment increased total bilirubin concentration (median 6.95 μmol/L vs. 8.55, + 23.02%; p < 0.001), but did not change plasma HMOX1 mRNA and HMOX1 protein concentrations. Plasma concentrations of OxLDL (- 31.85%, p < 0.001), MCP-1 (- 16.20%, p = 0.020) and CRP (- 7.32%, p = 0.010) were decreased but MDA was not decreased (15.32%, p = 0.107). Within subjects, increment of plasma bilirubin concentration did not correlate with the changes in HMOX1 mRNA and protein concentrations, but correlated with low-density lipoprotein cholesterol decrement (r = - 0.374, p = 0.012). Bilirubin increment did not correlate with the changes in oxidative and inflammatory markers.
Our prospective observational trial finally confirms that atorvastatin (20 mg/day for 10 weeks) increases plasma total bilirubin concentration. However, it seems that this effect is HMOX1-independent.
体外和动物研究表明,他汀类药物可增加血红素加氧酶-1基因(HMOX1)的表达,据此推测,这会增加血浆胆红素浓度。然而,目前缺乏他汀类药物同时增加HMOX1表达和血浆胆红素浓度的临床证据。我们假设,对于稳定型心绞痛患者,阿托伐他汀治疗(20毫克/天,持续10周)会同时增加总胆红素浓度和HMOX1表达,通过血浆分析进行无创评估。
对44例稳定型心绞痛患者在他汀类药物治疗前后测量血浆总胆红素、HMOX1 mRNA和HMOX1蛋白浓度,以及氧化型低密度脂蛋白(OxLDL)、丙二醛(MDA)、单核细胞趋化蛋白(MCP-1)和C反应蛋白(CRP)的血浆浓度。
阿托伐他汀治疗使总胆红素浓度升高(中位数6.95微摩尔/升对8.55,+23.02%;p<0.001),但未改变血浆HMOX1 mRNA和HMOX1蛋白浓度。OxLDL(-31.85%,p<0.001)、MCP-1(-16.20%,p=0.020)和CRP(-7.32%,p=0.010)的血浆浓度降低,但MDA未降低(15.32%,p=0.107)。在受试者体内,血浆胆红素浓度的升高与HMOX1 mRNA和蛋白浓度的变化无关,但与低密度脂蛋白胆固醇的降低相关(r=-0.374,p=0.012)。胆红素的升高与氧化和炎症标志物的变化无关。
我们的前瞻性观察性试验最终证实,阿托伐他汀(20毫克/天,持续10周)可增加血浆总胆红素浓度。然而,这种作用似乎与HMOX1无关。