The Journal of international medical research · 2005
Hydroxyethyl starch inhibits intestinal production of cytokines and activation of transcription factors in endotoxaemic rats.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lv R, Zhou W, Yang J J, Jin Y, Xu J G
Аннотация
We studied the effect of hydroxyethyl starch (HES) on intestinal production of cytokines and activation of transcription factors in sepsis. Septic rats, induced by intraperitoneal lipopolysaccharide (LPS) (5 mg/kg), were treated with intravenous HES (16 ml/kg) or saline (64 ml/kg). Rat ileal tissues were collected at 2 h, 3 h or 6 h after LPS challenge. Levels of tumour necrosis factor alpha (TNF-alpha), interleukin (IL) 1beta, IL-6, IL-8 and IL-10, cytokine mRNAs, activities of nuclear factor kappa-B (NF-KB) and activator protein-1 (AP-1), and the number of ileal myeloperoxidase (MPO)-positive cells were determined for each group. HES significantly reduced the LPS-induced increase in intestinal levels of TNF-alpha, IL-1beta, IL-6, IL-8 and their corresponding mRNAs. HES also decreased the number of MPO-positive cells induced by LPS and inhibited activation of NF-kappaB and AP-1. The results suggest that in sepsis, HES may down-regulate intestinal pro-inflammatory cytokine production via suppression of NF-kappaB and AP-1 activation.
Предметные рубрики MeSH
AnimalsCytokinesDNA PrimersDNA, ComplementaryDown-RegulationEndotoxemiaHydroxyethyl Starch DerivativesIleumImmunohistochemistryInterleukin-1Interleukin-10Interleukin-6Interleukin-8Intestinal MucosaIntestinesLipopolysaccharidesMaleNF-kappa BPeroxidasePlasma SubstitutesRNA, MessengerRatsRats, Sprague-DawleySepsisTime FactorsTranscription Factor AP-1Transcription FactorsTumor Necrosis Factor-alpha