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首页> 外文期刊>Archives of Toxicology >VEGF isoforms and receptors expression throughout acute acetaminophen-induced liver injury and regeneration
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VEGF isoforms and receptors expression throughout acute acetaminophen-induced liver injury and regeneration

机译：整个对乙酰氨基酚引起的肝损伤和再生中的VEGF亚型和受体表达

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Acetaminophen (APAP) is a widely-used analgesic and a known hepatotoxic agent. Vascular endothelial growth factor (VEGF) is a growth factor with multiple functional roles. VEGF plays an important role in angiogenesis and hepatic regeneration. The aim of this study was to determine the expression of VEGF isoforms and its receptors throughout liver regeneration after the administration of a toxic dose of APAP in rats. Ten groups of adult male rats received a dose of 3.5 g/kg b.w. of APAP per os. The rats were killed post administration at 0–288 h. Blood and liver tissue were extracted. Determination of serum transaminases and alkaline phophatase activities was performed. Liver injury and regeneration were assessed with hematoxylin-eosin specimens, morphometric analysis, hepatic thymidine kinase assay and Ki-67 expression. Reverse transcription-polymerase chain reaction and immunohistochemical methods were used for assessment of VEGF isoforms and receptors differential expression. High activities of aspartate aminotransferase were observed at 24 and 36 h with another peak of activity at 192 h post administration. Alanine aminotransferase was highest at 36 h. Alkaline phophatase was increased post 24 h being higher at 72,192 and 240 h. Centrilobular necrosis was observed at 48–72 h and thorough restoration of the liver microarchitecture was observed at 288 h. Liver regeneration lasted from 24–192 h according to the results from thymidine kinase activity and Ki-67 expression. VEGF and VEGF receptor-2 m-RNA levels presented with a three-peak pattern of expression at 12–24, 72–96 and 192–240 h post administration. Significant difference was noted between periportal and centrilobular immunohistochemical expression. VEGF proves to play a critical role during APAP-induced liver regeneration as it presents with three points of higher expression. The first two time points are associated with the initial inflammatory reaction to the noxious stimulus and the hepatocyte regenerative process where as the third one is indicative of the potential involvement of VEGF in processes of remodeling
机译：对乙酰氨基酚（APAP）是一种广泛使用的止痛药，也是已知的肝毒性药物。血管内皮生长因子（VEGF）是具有多种功能的生长因子。 VEGF在血管生成和肝再生中起重要作用。这项研究的目的是确定在大鼠中毒性剂量的APAP给药后整个肝脏再生过程中VEGF亚型及其受体的表达。十组成年雄性大鼠的剂量为3.5 g / kg b.w.每个操作系统的APAP。给药后0-288小时处死大鼠。提取血液和肝组织。进行血清转氨酶和碱性磷酸酶活性的测定。用苏木精-伊红标本，形态分析，肝胸苷激酶测定和Ki-67表达评估肝损伤和再生。逆转录-聚合酶链反应和免疫组化方法用于评估VEGF亚型和受体的差异表达。在给药后24和36小时观察到天冬氨酸转氨酶的高活性，在给药后192小时有另一个活性峰值。丙氨酸氨基转移酶在36 h时最高。碱性磷酸酶在24小时后增加，在72,192和240小时时更高。在48-72小时观察到小叶中心坏死，在288小时观察到肝微结构彻底恢复。根据胸苷激酶活性和Ki-67表达的结果，肝脏的再生持续24至192小时。给药后12–24、72–96和192–240 h，VEGF和VEGF受体2 m-RNA水平呈三峰表达模式。注意到门静脉周围和小叶的免疫组织化学表达之间的显着差异。 VEGF被证明在APAP诱导的肝再生过程中起关键作用，因为它具有三个更高的表达点。前两个时间点与有害刺激的初始炎症反应和肝细胞再生过程有关，而第三个时间点表明VEGF可能参与了重塑过程

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