Susceptibility of Lewis and Fischer rats to stress-induced worsening of TNB-colitis:: protective role of brain CRF
Susceptibility of Lewis and Fischer rats to stress-induced worsening of TNB-colitis:: protective role of brain CRF
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DOI：
10.1152/ajpgi.1999.276.4.g1027
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发表时间：
1999-04-01
影响因子：
4.5
通讯作者：
Anton, P
中科院分区：
文献类型：
--
作者：
Million, M;Taché, Y;Anton, P
我们评估了中枢促肾上腺皮质激素释放因子(CRF)在应激诱导的结肠炎恶化中的作用：在CRF对应激反应低(Lewis/N)和高(Fischer 344/N)的近交系大鼠中。结肠内注射2，4，6-三硝基苯磺酸(TNB)在第7天通过宏观评分、组织学评估、组织髓过氧化物酶(MPO)活性以及摄食量和体重减少来评估两种菌株诱导的相似严重程度的结肠炎。两个菌株的结肠炎均可通过每日脑室注射CRF来抑制。慢性应激(每天3h，隔日禁水或束缚6d)对Lewis大鼠结肠炎的加重作用大于Fischer大鼠(MPO活性分别增加71%和22%)。侧脑室注射CRF拮抗剂ASTRESIN增强了结肠炎对应激的反应，并导致两个菌株的死亡。与Lewis相比，Fischer大鼠在单独应激后20min、TNB加应激后第1、3天血浆皮质酮水平升高。这些数据表明，中枢CRF抑制应激在实验性结肠炎中的促炎作用。
We assessed the role of central corticotropin-releasing factor (CRF) in stress-induced worsening of colitis :in inbred rat strains with hypo (Lewis/N) and hyper (Fischer344/N) CRF responses to stress. Intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid (TNB) induced colitis of similar severity in both strains as assessed on day 7 by macroscopic scoring, histological evaluation, tissue myeloperoxidase (MPO) activity, and decrease in food intake and body weight. Colitis was inhibited by daily intracerebroventricular injections of CRF in both strains. Chronic stress (3 h/day, water avoidance or wrap restraint on alternate days for 6 days) aggravated colitis more in Lewis than Fischer rats (71 and 22% further increase in MPO activity, respectively). The CRF antagonist astressin injected intracerebroventricularly enhanced the colitis response to stress and caused mortality in both strains. Fischer rats had higher plasma corticosterone levels 20 min after stress alone on day I and after TNB plus stress on days 1 and 3 compared with Lewis. These data show that central CRF restrains the proinflammatory action of stress in experimental colitis.