Inhibition of interleukin-1 beta-induced pyresis in the rabbit by peptide 204-212 of lipocortin 5.

Inhibition of interleukin-1 beta-induced pyresis in the rabbit by peptide 204-212 of lipocortin 5.
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脂皮质素 5 的肽 204-212 对白细胞介素 1 β 诱导的兔子发热的抑制。

DOI:
10.1016/0014-2999(95)00304-4
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发表时间:
1995
影响因子:
5
通讯作者:
L. Parente
L. Parente
中科院分区:
医学2区
文献类型:
--
作者:
M. Palmi;M. Frosini;G. Sgaragli;C. Becherucci;M. Perretti;L. Parente

文献摘要

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侧脑室注射白细胞介素-1 β(12.5ng/kg)后,脑脊液中前列腺素E_2浓度迅速升高(+632.6 ± 243.9%),体温升高(+1.61 ± 0.14 Δ°C)。脑室内施用衍生自脂皮质素5的抗炎九肽(氨基酸204-212,SHLRKVFDK),此后称为脂皮质素5-(204-212)-肽,以显著的方式抑制脑脊液[前列腺素E2]的增加和由细胞因子诱导的发热反应。这种抑制作用可能是由于肽干扰磷脂酶A2的活性。由随机改组序列中的相同氨基酸形成的对照肽(FKRVHDLKS)没有影响。这些结果表明,除了先前报道的抗炎作用之外,脂皮质素5的肽204-212与糖皮质激素一样具有解热活性。对脂皮质素衍生肽的研究可能会导致新的抗炎和解热化合物的开发。
The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E2concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from lipocortin 5, thereafter referred to as lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E2] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A2activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.