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仅乙醛就可能在急性酒精性肝病中引发肝细胞损伤。

Acetaldehyde alone may initiate hepatocellular damage in acute alcoholic liver disease.

作者信息

Barry R E, McGivan J D

出版信息

Gut. 1985 Oct;26(10):1065-9. doi: 10.1136/gut.26.10.1065.

Abstract

Acetaldehyde may be the injurious agent in acute alcoholic liver disease. It has been suggested that the mechanism of liver injury in this situation may be immunologically mediated. In the present study acetaldehyde has been bound to human liver plasma membranes. The activation of C3 by the acetaldehyde/membrane product was measured by immunofixation of the separated C3 components. Activation of C3 by acetaldehyde exposed liver plasma membranes was increased to 16.4% compared with 6% by non-exposed membranes (p = 0.004). Human liver plasma membranes bound 212 +/- 18 nmol acetaldehyde per mg membrane protein. The binding constant was 439 +/- 81 microM. It is concluded that acetaldehyde bound to human liver plasma membranes activates the complement sequence and this may be the initial stage in the pathogenesis of acute alcoholic liver disease.

摘要

乙醛可能是急性酒精性肝病中的损伤因子。有人提出,在这种情况下肝损伤的机制可能是免疫介导的。在本研究中,乙醛已与人肝细胞膜结合。通过对分离的C3成分进行免疫固定来测定乙醛/膜产物对C3的激活作用。与未暴露的膜相比,乙醛暴露的肝细胞膜对C3的激活作用增加到16.4%,而未暴露膜的激活率为6%(p = 0.004)。人肝细胞膜每毫克膜蛋白结合212±18 nmol乙醛。结合常数为439±81 μM。得出的结论是,与人肝细胞膜结合的乙醛激活补体序列,这可能是急性酒精性肝病发病机制的初始阶段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51d3/1432946/7964873c1a77/gut00383-0100-a.jpg

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