麦角胺对牛的抗炎作用。

N. Filipov, F. N. Thompson, J. A. Stuedemann, T. Elsasser, S. Kahl, L. Stanker, C. Young, D. Dawe, C. K. Smith
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引用次数: 9

摘要

本试验旨在研究麦角生物碱麦角胺(ET)是否会改变牛对内毒素(LPS)的反应。麦角生物碱是一种用于模拟牛羊茅中毒的生物碱。16只实验组分为对照组(C)、麦角胺组(ET)、内毒素组(LPS)和内毒素组(ET + LPS)。ET组和ET + LPS组给予单次静脉注射ET (40 μ g)。公斤。体wt(-1)),而C组和LPS组接受单次注射无菌载体。在给药30分钟后,单次静脉注射LPS(0.2微克)。公斤。给出体wt(-1)。在48小时后的不同时间点采集血液。内毒素升高直肠温度(RT)和循环中肿瘤坏死因子- α (tnf - α)、皮质醇、触珠蛋白(Hp)、血栓素B(TXB)的水平。与ET + LPS相比,经ET预处理后,循环Hp、tnf - α和TXB(2)的增加被减弱。麦角胺本身增加循环皮质醇和RT,而降低血清催乳素(PRL)。因此,虽然以0.2微克/千克的剂量给牛LPS会产生预期的反应,但ET + LPS的组合会减弱单独使用LPS的主要影响。因此,急性给药ET似乎具有抗炎作用,因为它降低了对LPS的炎症反应,这种效果可能至少部分是由ET引起的皮质醇增加引起的。
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Anti-inflammatory effects of ergotamine in steers.
The objective of this experiment was to investigate whether the ergot alkaloid, ergotamine (ET), an alkaloid used to model fescue toxicosis in cattle, modifies the response of cattle to endotoxin (LPS) challenge. Steers (n = 16) were divided into the following treatment groups: control (C), ergotamine (ET), endotoxin (LPS), and ET + LPS. ET and ET + LPS groups received a single bolus intravenous injection of ET (40 microg. kg. body wt(-1)), whereas C and LPS steers received a single bolus injection of sterile vehicle. Thirty minutes after ET/vehicle administration, a single bolus intravenous injection of LPS (0.2 microg. kg. body wt(-1)) was given. Blood was collected at various time points for 48 hr post. Endotoxin increased rectal temperature (RT) and the circulating levels of tumor necrosis factor-alpha (TNF-alpha), cortisol, haptoglobin (Hp), thromboxane B(2) (TXB(2)). The circulating Hp, TNF-alpha, and TXB(2) increases were blunted by pretreatment with ET compared with ET + LPS. Ergotamine by itself increased circulating cortisol and RT, whereas it decreased serum prolactin (PRL). Therefore, whereas administration of LPS at 0.2 microg/kg to steers resulted in an expected response, the combination of ET + LPS attenuated major effects of LPS alone. Thus, acute administration of ET appeared to be anti-inflammatory as it decreased the inflammatory response to LPS, an effect likely driven at least in part by the ET-caused cortisol increase.
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