Evidence of a role for galectin‐1 in acute inflammation

Evidence of a role for galectin‐1 in acute inflammation
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DOI:
10.1002/(sici)1521-4141(200005)30:5
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发表时间:
2000-05
影响因子:
5.4
通讯作者:
G. Rabinovich;C. Sotomayor;C. Riera;I. Bianco;S. Correa
G. Rabinovich;C. Sotomayor;C. Riera;I. Bianco;S. Correa
中科院分区:
医学3区
文献类型:
--
作者:
G. Rabinovich;C. Sotomayor;C. Riera;I. Bianco;S. Correa

文献摘要

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半乳糖凝集素-1(Galectin-1,Gal-1)是β-半乳糖苷结合蛋白家族的成员,已被认为在免疫和炎症过程中发挥关键作用。本研究通过大鼠后爪水肿试验探讨了Gal-1在急性炎症中的体内作用概念。当在蜂毒磷脂酶A2(PLA 2)注射前30分钟或与PLA 2一起共注射时,局部给予Gal-1(0.5、2、4和8 μg / ml)可抑制蜂毒磷脂酶A2(PLA 2)诱导的急性炎症。抗炎作用被特异性抗体阻止,但与其碳水化合物结合特性无关。相反,Gal-1不能抑制组胺诱导的水肿。组织学研究显示,当在PLA 2之前注射Gal-1时,炎症过程明显减少,这由浸润的多形核中性粒细胞数量减少和脱颗粒肥大细胞稀少证明。还在体外评估了抗炎作用,表明Gal-1处理减少了刺激的腹膜巨噬细胞的前列腺素E2分泌和花生四烯酸释放。本文提供的结果为Gal-1在急性炎症中的作用提供了第一个证据,并表明抗炎作用涉及抑制炎症反应的可溶性和细胞介质。
Galectin‐1 (Gal‐1), a member of a family of β‐galactoside‐binding proteins, has been suggested to play key roles in immunological and inflammatory processes. The present study deals with the concept of an in vivo role for Gal‐1 in acute inflammation by using the rat hind paw edema test. Local administration of Gal‐1 (0.5, 2, 4 and 8 μg / ml) inhibited acute inflammation induced by bee venom phospholipase A2 (PLA2) when it was injected 30 min before the enzyme or co‐injected together with PLA2. The anti‐inflammatory effect was prevented by a specific antibody, but independent of its carbohydrate‐binding properties. In contrast, Gal‐1 failed to inhibit histamine‐induced edema. Histopathological studies showed a clear reduction of the inflammatory process when Gal‐1 was injected before PLA2, evidenced by a diminished number of infiltrated polymorphonuclear neutrophils and scarce degranulated mast cells. The anti‐inflammatory effect was also assessed in vitro, showing that Gal‐1 treatment reduced prostaglandin E2 secretion and arachidonic acid release from stimulated peritoneal macrophages. Results presented here provide the first evidence for a role of Gal‐1 in acute inflammation and suggest that the anti‐inflammatory effect involves the inhibition of both soluble and cellular mediators of the inflammatory response.