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机构地区:[1]兰州大学第一医院重症医学科,730000 [2]成都医学院体温与炎症四川省高校重点实验室,610500
出 处:《医学研究杂志》2017年第11期76-80,共5页Journal of Medical Research
基 金:四川省教育厅科研基金资助项目(15ZA0251)
摘 要:目的研究外周给精氨酸加压素(AVP)对脂多糖(LPS)引起大鼠发热和棕色脂肪产热以及血清中IL-1β和PGE2水平的变化。方法实验用成年雄性SD大鼠,在23℃环境温度下,明暗时间各12h。用无线遥测系统连续测量大鼠体核温度(Tc)、棕色脂肪温度(T_(BAT))和活动。10:00时或11:30时分别给大鼠腹腔注射LPS(50μg/kg)、AVP(10μg/kg)或V1a受体阻断剂(30μg/kg)。用ELISA法测定血清IL-1β和PGE_2的含量。结果腹腔注射LPS后TBAT升高出现在Tc升高之前。腹腔V1a受体阻断剂能提高LPS引起发热反应。AVP能抑制LPS引起发热大鼠血清中IL-lβ和PGE2水平升高反应。结论 BAT产热在LPS引起的发热中有重要的作用。外周给AVP可通过抑制棕色脂肪产热和降低血液中IL-lβ和PGE2的浓度而翻转LPS发热反应。内源性AVP也有限制LPS发热的作用。Objective To investigate the effect of peripheral administration of arginine vasopressin (AVP) on lipopolysaccharide (LPS)-induced fever in the rats, and its relationship with the change in brown adipose tissue (BAT) thermogenesis and Interleukine-1β (IL-1β) and prostaglandin E2 (PGE2).Methods The core temperature (Tc),BAT temperature (TBAT) and activity were measured by telemetry in adult male Sprague-Dawley rats at an ambient temperature of 23℃ during a 12h light:12h dark photoperiod (lights on at 06:00 and lights off at 18:00). The rats were dosed intraperitoneally with LPS (50μg/kg), AVP (10μg/kg) or V1a vasopressin receptor antagonist (V1a antagonist, 30μg/kg) at 10:00 or 10:30. The concentrations of IL-1β and PGE2 in serum were tested by ELISA.Results (1) The increases in TBAT following LPS preceded the increases in Tc. (2) Peripheral administration of AVP reversed LPS-induced fever and decreased BAT thermogenesis. (3) V1a antagonist enhanced the fever produced by LPS. (4) AVP could significantly attenuate LPS-induced IL-1β and PGE2 production.Conclusion (1) BAT thermogenesis plays an important role in LPS-induced fever. (2) Peripheral administration of AVP reversed LPS-induced fever by reduction of BAT thermogenesis and inhibition of IL-1β and PGE2. (3) Endogenous AVP can attenuate fever induced by LPS.
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