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Human C-reactive protein enhances vulnerability of immature rats to hypoxic-ischemic brain damage: a preliminary study.

Authors: Kinugasa-Taniguchi, Y  Tomimatsu, T  Mimura, K  Kanagawa, T  Shimoya, K  Murata, Y  Kimura, T 
Citation: Kinugasa-Taniguchi Y, etal., Reprod Sci. 2010 May;17(5):419-25. doi: 10.1177/1933719110361379. Epub 2010 Mar 10.
Pubmed: (View Article at PubMed) PMID:20220110
DOI: Full-text: DOI:10.1177/1933719110361379

In utero exposure to infection or inflammation is a strong and independent predictor of cerebral palsy. Using a rat model of neonatal hypoxic-ischemic (HI) encephalopathy, we investigated the hypothesis that C-reactive protein (CRP), which is not specific for infection, aggravates vulnerability of the immature brain to HI. Seven-day-old rats were divided into human CRP treated and control groups. After injection of each solution, they underwent left common carotid artery ligation and exposure to 8% hypoxia for 40 minutes. Human CRP, rat CRP, and interleukin 6 (IL-6) concentrations in serum were measured by enzyme-linked immunosorbent assay 30 to 60 minutes after injection of each solution. Four days later, microtubule-associated protein 2 (MAP-2) immunostaining was used to examine the brains for neuronal damage. Human CRP treatment significantly reduced the MAP-2 positive area ratio, compared with control group ( P < .05), suggesting that human CRP-enhanced susceptibility to HI-induced brain damage. Mean serum human CRP concentration in the human CRP group was 1823 +/- 520 ng/mL (range: 365-3964 ng/mL). Interleukin 6 concentrations in serum were moderately elevated in both groups, without significant differences, and rat CRP concentrations were within normal range. C-reactive protein makes the immature brain susceptible to HI insult, even if the insult causes little or no injury by itself.


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RGD Object Information
RGD ID: 9585994
Created: 2014-09-24
Species: All species
Last Modified: 2014-09-24
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.