乙醇对再生神经载脂蛋白的合成与分泌的影响

Effects of Ethanol on Synthesis and Secretion of Apolipoproteins by Regenerating Nerve

本文检测了再生神经释放载脂蛋白Ｅ和Ａ１的量。把从含有乙醇的液体饲料喂养的大白鼠取得的再生神经，切成较小的节段培养后，测得释放入培养基中的载脂蛋白Ｅ（ａｐｏＥ）的量，仅仅只有对照组的５０％，而载脂蛋白Ａ１（ａｐｏＡ１）的量几乎是对照组的２００％。释放入培养基中ａｐｏＥ减少的程度与神经中ｍＲＮＡ减少的程度一致。这样，慢性乙醇摄入影响再生神经ａｐｏＥ的合成是通过改变它的ｍＲＮＡ的水平所致。另一方面，ａｐｏＡ１的ｍＲＮＡ在实验组和对照组的神经中均不能检测出。由再生神经释放入培养基中的ａｐｏＡ１与培养前所含的量没有明显的差异。因此，由损伤神经释放的ａｐｏＡ１很可能是从血流而来的。而乙醇喂养的老鼠损伤神经中ａｐｏＡ１含量的增加，是由于增强了神经———血液屏障的通透性。载脂蛋白在损伤神经中的堆积很可能在神经再生过程中扮演一个重要的角色。

The amounts of apolipoprotein(apoE) and A 1 were examined in regenerating nerve.Cultured minced segments of regenerating nerve taken from rats fed an alcohol containing liquid diet released only 50% of apoE but nearly 200% of apoA 1 when compared with a control diet.The extent of decrease in medium apoE mRNA in the nerve.Thus,chronic ethanol ingestion affects apoE synthesis of regenerating nerve by changing its mRNA.On the other hand,apoA 1 mRNA couldn't detected from both groups.The amount of apoA 1 released by regenerating nerve was not significantly lager than that present in the nerve tissue prior to incubation.Therefore,apoA 1 released by the injured nerve may originate from the bloodstream.The increase in apoA 1 content in the injured nerve of alcoholic fed rats is due to an enhanced permeability of the nerve blood barrier.The burst of apo in the injured nerve is likely to play a role in nerve regeneration.The perturbation of apo contents in regenerating nerve by chronic ethanol consumption may relate to the pathogenesis of alcoholic neuropathy.