Oxidized low-density-lipoprotein accumulation is associated with liver fibrosis in experimental cholestasis.

Oxidized low-density-lipoprotein accumulation is associated with liver fibrosis in experimental cholestasis.
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氧化的低密度脂蛋白积累与实验性胆汁淤积中的肝纤维化有关。

DOI:
10.1590/s1807-59322008000400020
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发表时间:
2008-08
期刊:
Clinics (Sao Paulo, Brazil)
影响因子:
--
通讯作者:
Cömert M
Cömert M
中科院分区:
其他
文献类型:
--
作者:
Karadeniz G;Acikgoz S;Tekin IO;Tascýlar O;Gun BD;Cömert M

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本研究的目的是探讨胆汁淤积大鼠oxLDL的积累和肝纤维化之间的可能关系。越来越多的证据支持氧化应激导致脂质过氧化反应参与胆汁淤积性肝损伤和肝纤维化的发病机制。氧化低密度脂蛋白(OxLDL)是一种主要的早期脂质过氧化产物,被认为在各种免疫炎症机制中起着复杂的作用。对Wistar白化大鼠进行了长时间(21天)的实验性胆管结扎。对胆管结扎大鼠(n = 8)和假手术大鼠(n = 8)进行血液生化分析、肝脏组织病理学评价、肝组织匀浆中丙二醛(MDA)和超氧化物歧化酶(SOD)浓度测定以及肝组织中oxLDL的免疫荧光染色。与假手术组相比,黄疸组大鼠肝组织中MDA含量显著升高,SOD含量显著降低。在黄疸大鼠的肝组织切片中也观察到阳性oxLDL染色。组织学检查表明,没有纤维化或肝细胞损伤的其他迹象中发现假手术组,而严重的肝细胞损伤的功能,特别是纤维化,发现黄疸大鼠。我们的研究结果支持这样的发现,即oxLDL在氧化应激加剧期间作为中间剂产生,或者它们以其他方式促进肝纤维化过程的各种病理机制。无论机制如何,很明显,oxLDL水平升高与肝细胞损伤,特别是与纤维化之间存在关联。需要进一步的研究来评估oxLDL对继发性胆汁性肝硬化进展的潜在影响。
The aim of the present study was to examine the probable relationship between the accumulation of oxLDL and hepatic fibrogenesis in cholestatic rats. There is growing evidence to support the current theories on how oxidative stress that results in lipid peroxidation is involved in the pathogenesis of cholestatic liver injury and fibrogenesis. One of the major and early lipid peroxidation products, OxLDL, is thought to play complex roles in various immuno-inflammatory mechanisms. A prolonged (21-day) experimental bile duct ligation was performed on Wistar-albino rats. Biochemical analysis of blood, histopathologic evaluation of liver, measurement of the concentration of malondialdehyde (MDA) and superoxide-dismutase (SOD) in liver tissue homogenates, and immunofluorescent staining for oxLDL in liver tissue was conducted in bile-duct ligated (n = 8) and sham-operated rats (n = 8). Significantly higher levels of MDA and lower concentrations of SOD were detected in jaundiced rats than in the sham-operated rats. Positive oxLDL staining was also observed in liver tissue sections of jaundiced rats. Histopathological examination demonstrated that neither fibrosis nor other indications of hepatocellular injury were found in the sham-operated group, while features of severe hepatocellular injury, particularly fibrosis, were found in jaundiced rats. Our results support the finding that either oxLDLs are produced as an intermediate agent during exacerbated oxidative stress or they otherwise contribute to the various pathomechanisms underlying the process of liver fibrosis. Whatever the mechanism, it is clear that an association exists between elevated oxLDL levels and hepatocellular injury, particularly with fibrosis. Further studies are needed to evaluate the potential effects of oxLDLs on the progression of secondary biliary cirrhosis.
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发表时间: 2006-02-01
影响因子: 4
作者:
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发表时间: 2003-04-01
期刊: VIRCHOWS ARCHIV
影响因子: 3.5
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Costa, AMA;Tuchweber, B;Desmoulière, A
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DOI: 10.1016/s0021-9150(01)00646-3
发表时间: 2002-04-01
期刊: ATHEROSCLEROSIS
影响因子: 5.3
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