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Taurine suppresses oxidative stress-potentiated expression of lectin-like oxidized low-density lipoprotein receptor and restenosis in balloon-injured rabbit iliac artery

机译:牛磺酸抑制了凝胶状氧化低密度脂蛋白受体的氧化胁迫调节表达,并在气球伤害兔髂动脉中的再狭窄

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摘要

1. In endothelial cells, the major receptor for the binding and internalization of oxidized low-density lipoprotein (LDL) is the lectin-like oxidized LDL receptor (LOX-1). The aim of the present study was to investigate the effects of taurine on intimal thickening and LOX-1 expression under normal and oxidative conditions. 2. The iliac artery of rabbits were subjected to balloon injury and oxidative stress was induced by 14days treatment of rabbits with 75mg/kg, s.c., buthionine sulfoximine (BSO), a specific inhibitor of glutathione synthesis. Taurine was administered in drinking water (1%, w/v) for 14days in the presence (BSO+Taurine group) and in the absence of BSO treatment (Taurine group). In taurine and placebo groups, rabbits were injected with 4mL, s.c., 0.9% NaCl (vehicle for BSO) for 14days. 3. Taurine (1% in drinking water, w/v) preserved plasma levels of anti-oxidants and lowered the increased blood pressure induced by BSO. The stenosis rate of 29.92% in the placebo group increased to 72.20% in the BSO group, which was significantly reduced to 42.21% by taurine (P<0.001; n=5). Localization of LOX-1 to the intima and media of the iliac artery was demonstrated in the present study. Taurine treatment reduced the BSO-induced increase in LOX-1 expression at both the protein and mRNA levels (P<0.05 and P<0.01, respectively). 4. The results demonstrate that the stenosis rate and LOX-1 expression correlate well with oxidative status. Manipulation of LOX-1 expression by taurine may have therapeutic benefits in preventing restenosis.
机译:在内皮细胞中,氧化低密度脂蛋白(LDL)的结合和内化的主要受体是凝集素状的氧化LDL受体(LOX-1)。本研究的目的是研究牛磺酸对正常和氧化条件下的牛磺酸对内膜增稠和LOX-1表达的影响。 2.兔的髂动脉受到球囊损伤,14天治疗兔的氧化胁迫诱导,具有75mg / kg,S.C.,甲硫氨酸亚磺酰昔亚胺(BSO),谷胱甘肽合成的特异性抑制剂。在存在(BSO + Taurine Group)和没有BSO治疗(牛磺酸基团)的情况下,牛磺酸在饮用水(1%,w / v)中给药14天。在牛磺酸和安慰剂组中,兔子注射4ml,S.C.,0.9%NaCl(BSO载体)14天。 3.牛磺酸(饮用水1%,W / V)保存血浆抗氧化剂水平,降低了BSO诱导的血压增加。 BSO组中,安慰剂组中29.92%的狭窄率增加到72.20%,牛磺酸的42.21%显着降至42.21%(P <0.001; n = 5)。在本研究中证明了LOX-1的定位和髂动脉的内部和培养基。牛磺酸治疗在蛋白质和mRNA水平下降低了BSO诱导的LOX-1表达增加(分别为P <0.05和P <0.01)。 4.结果表明,狭窄速率和LOX-1表达与氧化地位好。牛磺酸的LOX-1表达的操纵可能具有治疗效果,防止再狭窄。

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