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肝细胞生长因子可加速大鼠急性缺血性肾损伤的恢复。

Hepatocyte growth factor accelerates recovery from acute ischemic renal injury in rats.

作者信息

Miller S B, Martin D R, Kissane J, Hammerman M R

机构信息

George M. O'Brien Kidney and Urological Diseases Center, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.

出版信息

Am J Physiol. 1994 Jan;266(1 Pt 2):F129-34. doi: 10.1152/ajprenal.1994.266.1.F129.

Abstract

Effects of hepatocyte growth factor (HGF) administration were examined in a model of acute ischemic renal injury induced by bilateral renal artery occlusion in rats. Compared with rats administered vehicle, rats administered 20 micrograms HGF subcutaneously 30 min postischemia had significantly lower serum creatinine and blood urea nitrogen levels over the course of 7 days postocclusion, enhanced insulin clearances measured on day 2 postocclusion, reduced mortality, and much less injury evident by examination of kidney histologies 7 days postinjury. The tubular regeneration that occurred postischemic injury was reflected by increased incorporation of 5-bromo-2'-deoxyuridine (BrdU) in cortical tubular epithelium compared with incorporation in kidneys from noninjured rats. HGF enhanced BrdU incorporation compared with vehicle, indicating enhanced mitogenesis. The weight loss that occurs postischemic injury was not ameliorated by the dose of HGF we employed. We conclude that administration of HGF postischemic injury to rats stimulates the recovery of normal kidney function and the regeneration of proximal tubular epithelium.

摘要

在大鼠双侧肾动脉闭塞诱导的急性缺血性肾损伤模型中,研究了肝细胞生长因子(HGF)给药的效果。与给予赋形剂的大鼠相比,在缺血后30分钟皮下注射20微克HGF的大鼠,在闭塞后7天内血清肌酐和血尿素氮水平显著降低,在闭塞后第2天测得的胰岛素清除率提高,死亡率降低,并且在损伤后7天通过肾脏组织学检查可见损伤明显减轻。与未受伤大鼠的肾脏相比,缺血性损伤后发生的肾小管再生表现为皮质肾小管上皮中5-溴-2'-脱氧尿苷(BrdU)掺入增加。与赋形剂相比,HGF增强了BrdU掺入,表明有丝分裂增强。我们使用的HGF剂量并未改善缺血性损伤后出现的体重减轻。我们得出结论,对大鼠缺血性损伤后给予HGF可刺激正常肾功能的恢复和近端肾小管上皮的再生。

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