Scalabrino Giuseppe, Peracchi Maddalena
Institute of General Pathology and Centre of Excellence on Neurodegenerative Diseases, University of Milan, Via Mangiagalli 31, I-20133 Milano, Italy.
Trends Mol Med. 2006 Jun;12(6):247-54. doi: 10.1016/j.molmed.2006.04.008. Epub 2006 May 11.
Cobalamin-deficient (Cbl-D) central neuropathy in the rat is associated with a locally increased expression of neurotoxic tumour necrosis factor-alpha (TNF-alpha) and a locally decreased expression of neurotrophic epidermal growth factor (EGF). These recent findings suggest that cobalamin oppositely regulates the expression of TNF-alpha and EGF, and raise the possibility that these effects might be independent of its coenzyme function. Furthermore, adult Cbl-D patients have high levels of TNF-alpha and low levels of EGF in the serum and cerebrospinal fluid. Serum levels of TNF-alpha and EGF of cobalamin-treated patients normalize concomitantly with haematological disease remission. These observations suggest that cobalamin deficiency induces an imbalance in TNF-alpha and EGF levels in biological fluids that might have a role in the pathogenesis of the damage caused by pernicious anaemia.
大鼠体内的钴胺素缺乏（Cbl-D）中枢神经病变与神经毒性肿瘤坏死因子-α（TNF-α）局部表达增加以及神经营养性表皮生长因子（EGF）局部表达减少有关。这些最新发现表明，钴胺素对TNF-α和EGF的表达具有相反的调节作用，并增加了这些作用可能独立于其辅酶功能的可能性。此外，成年Cbl-D患者血清和脑脊液中的TNF-α水平较高，EGF水平较低。接受钴胺素治疗的患者血清中TNF-α和EGF水平会随着血液系统疾病的缓解而恢复正常。这些观察结果表明，钴胺素缺乏会导致生物体液中TNF-α和EGF水平失衡，这可能在恶性贫血所致损伤的发病机制中起作用。
