Ishibashi S, Yamada N, Oka Y, Shimano H, Mori N, Yoon T H, Shimada M, Kanazawa Y, Akanuma Y, Murase T
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Biochem Biophys Res Commun. 1988 Aug 30;155(1):283-8. doi: 10.1016/s0006-291x(88)81081-7.
To elucidate the pathogenesis of diabetic neuropathy, synthesis and secretion of apolipoprotein E (apo E) from sciatic nerves after injury was studied in normal and streptozotocin-induced diabetic rats. Seven, 14, 28, 45 and 59 days after making crush injury on sciatic nerves with concomitant administration of streptozotocin (50 mg/kg body weight), the nerves were taken out and incubated with [35S]methionine. The [35S]labeled apo E was precipitated with specific antiserum. The amounts of apo E secreted into medium by nerves of diabetic rats were 7 times greater than those of non-diabetic rats 7 days after injury. This enhanced secretion of apo E was relatively selective for this protein, since the ratio of the immunoprecipitable apo E to the TCA preciptitable protein in the medium increased in diabetic rats. Intriguing possibility deduced from these results is that the secretion of apo E is involved in the development of diabetic neuropathy.
为阐明糖尿病性神经病变的发病机制,我们在正常大鼠和链脲佐菌素诱导的糖尿病大鼠中研究了坐骨神经损伤后载脂蛋白E(apo E)的合成与分泌。在用链脲佐菌素(50 mg/kg体重)处理的同时,对坐骨神经造成挤压伤,分别于伤后7、14、28、45和59天取出神经,与[35S]甲硫氨酸一起孵育。[35S]标记的apo E用特异性抗血清沉淀。伤后7天,糖尿病大鼠神经分泌到培养基中的apo E量比非糖尿病大鼠高7倍。apo E的这种分泌增加对该蛋白具有相对选择性,因为培养基中免疫沉淀的apo E与三氯乙酸沉淀蛋白的比例在糖尿病大鼠中增加。从这些结果推断出的一个有趣的可能性是,apo E的分泌参与了糖尿病性神经病变的发展。