Lin R C, Miller B A, Mei M H, Ochs S, Lumeng L
Department of Medicine, Indiana University School of Medicine, Indianapolis.
Alcohol Clin Exp Res. 1992 Oct;16(5):899-903. doi: 10.1111/j.1530-0277.1992.tb01890.x.
The amounts of apolipoprotein (apo) E and A1 released into the culture medium were examined in the regenerating nerves distal to a crush site following chronic alcohol feeding. Cultured minced segments of regenerating nerves taken from rats fed an alcohol-containing liquid diet for 5 weeks released only 50% of apoE but nearly 200% of apoA1 when compared with rats pair-fed with a control diet. The extent of decrease in medium apoE corresponded to the decrease of apoE mRNA in the nerve. Thus, chronic alcohol ingestion affects apoE synthesis of regenerating nerves by changing its mRNA level. On the other hand, apoA1 mRNA remained undetectable in regenerating and intact nerves whether the rats were fed alcohol or not. Furthermore, the amount of apoA1 released by the regenerating nerve into the culture medium was not significantly larger than that present in the nerve tissue prior to incubation. Therefore, it is most likely that apoA1 released by the injured nerve originated from the bloodstream and the increase in apoA1 content seen in the crushed nerve of alcohol-fed rats is due to an enhanced permeability of the nerve-blood barrier. Since the burst of apolipoproteins in the injured nerve is likely to play a role in nerve regeneration, the perturbation of apolipoprotein contents in regenerating nerves by chronic alcohol consumption may contribute to the pathogenesis of alcoholic neuropathy.
在长期摄入酒精后，对挤压部位远端再生神经中释放到培养基中的载脂蛋白（apo）E和A1的量进行了检测。与喂食对照饮食的配对大鼠相比，取自喂食含酒精液体饮食5周的大鼠的再生神经培养切碎段释放的apoE仅为50%，而apoA1几乎为200%。培养基中apoE的降低程度与神经中apoE mRNA的降低相对应。因此，长期摄入酒精通过改变其mRNA水平影响再生神经中apoE的合成。另一方面，无论大鼠是否喂食酒精，在再生神经和完整神经中均未检测到apoA1 mRNA。此外，再生神经释放到培养基中的apoA1量并不显著大于孵育前神经组织中的量。因此，最有可能的是，受损神经释放的apoA1起源于血液，在喂食酒精的大鼠挤压神经中看到的apoA1含量增加是由于神经-血液屏障通透性增强所致。由于受损神经中载脂蛋白的爆发可能在神经再生中起作用，长期饮酒导致再生神经中载脂蛋白含量的扰动可能有助于酒精性神经病的发病机制。
