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急性炎症对维生素A充足大鼠肝脏和肾脏中血浆视黄醇、视黄醇结合蛋白及其mRNA的影响。

Effects of acute inflammation on plasma retinol, retinol-binding protein, and its mRNA in the liver and kidneys of vitamin A-sufficient rats.

作者信息

Rosales F J, Ritter S J, Zolfaghari R, Smith J E, Ross A C

机构信息

Department of Biochemistry, Medical College of Pennsylvania, Philadelphia 19129, USA.

出版信息

J Lipid Res. 1996 May;37(5):962-71.

PMID:8725149
Abstract

The acute inflammatory response to tissue injury and infection is associated with low concentrations of plasma retinol and its specific transport proteins, retinol-binding protein (RBP) and transthyretin (TTR). To examine the kinetics and mechanism of hyporetinemia, we have induced acute inflammation with lipopolysaccharide (LPS, from Pseudomonas aeruginosa) in rats with adequate stores of vitamin A. Twenty-four h after treatment with LPS (50 micrograms i.p. per 100 g body weight) or saline and food withdrawal, plasma retinol equalled 0.72 +/- 0.06 mumol/L (mean +/- SEM) in five LPS-treated rats versus 1.35 +/- 0.1 mumol/L in five saline-treated rats (P < 0.01). Plasma, liver, and kidney RBP and TTR concentrations were also significantly reduced, but liver and kidney retinol concentrations did not differ between treatment groups. The relative abundance of RBP mRNA in liver (LPS treatment compared to saline treatment) was reduced as early as 12 h (0.44 +/- 0.15, n = 4 pairs, P < 0.02), and continued to be reduced at 24 h (0.57 +/- 0.12, n = 5 pairs, P < 0.02). In the kidney this ratio did not change significantly due to LPS treatment. The relative abundance of cellular retinol-binding protein (CRBP) mRNA in liver and kidney also was not affected by LPS treatment. We infer from these data that inflammation-induced hyporetinemia results from a reduction in the hepatic synthesis of RBP and secretion of the retinol-RBP complex. Moreover, the results imply that plasma retinol concentration is a poor indicator of vitamin A status during inflammation.

摘要

对组织损伤和感染的急性炎症反应与血浆视黄醇及其特异性转运蛋白、视黄醇结合蛋白(RBP)和甲状腺素转运蛋白(TTR)的低浓度有关。为了研究低视黄醇血症的动力学和机制,我们在维生素A储备充足的大鼠中用脂多糖(LPS,来自铜绿假单胞菌)诱导急性炎症。在用LPS(每100克体重腹腔注射50微克)或生理盐水处理并禁食24小时后,5只LPS处理的大鼠血浆视黄醇浓度为0.72±0.06微摩尔/升(平均值±标准误),而5只生理盐水处理的大鼠为1.35±0.1微摩尔/升(P<0.01)。血浆、肝脏和肾脏中的RBP和TTR浓度也显著降低,但各治疗组之间肝脏和肾脏中的视黄醇浓度没有差异。肝脏中RBP mRNA的相对丰度(与生理盐水处理相比,LPS处理)早在12小时就降低了(0.44±0.15,n = 4对,P<0.02),并在24小时继续降低(0.57±0.12,n = 5对,P<0.02)。在肾脏中,该比例因LPS处理而无显著变化。肝脏和肾脏中细胞视黄醇结合蛋白(CRBP)mRNA的相对丰度也不受LPS处理的影响。我们从这些数据推断,炎症诱导的低视黄醇血症是由于肝脏中RBP合成减少和视黄醇-RBP复合物分泌减少所致。此外,结果表明,在炎症期间,血浆视黄醇浓度不是维生素A状态的良好指标。

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