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Abstract：
Dietary sphingolipids such as glucosylceramide (GlcCer) are potential nutritional factors associated with prevention of metabolic syndrome. Our current understanding is that dietary GlcCer is degraded to ceramide and further metabolized to sphingoid bases in the intestine. However, ceramide is only found in trace amounts in food plants and thus is frequently taken as GlcCer in a health supplement. In the present study, we successfully prepared konjac ceramide (kCer) using endoglycoceramidase I (EGCase I). Konjac, a plant tuber, is an enriched source of GlcCer (kGlcCer), and has been commercialized as a dietary supplement to improve dry skin and itching that are caused by a deficiency of epidermal ceramide. Nerve growth factor (NGF) produced by skin cells is one of the itch factors in the stratum corneum of the skin. Semaphorin 3A (Sema 3A) has been known to inhibit NGF-induced neurite outgrowth of epidermal nerve fibers. It is well known that the itch sensation is regulated by the balance between NGF and Sema 3A. In the present study, while kGlcCer did not show an in vitro inhibitory effect on NGF-induced neurite outgrowth of PC12 cells, kCer was demonstrated to inhibit a remarkable neurite outgrowth. In addition, the effect of kCer was similar to that of Sema 3A in cell morphological changes and neurite retractions, but different from C2-Ceramide. kCer showed a Sema 3A-like action, causing CRMP2 phosphorylation, which results in a collapse of neurite growth cones. Thus, it is expected that kCer is an advanced konjac ceramide material that may have neurite outgrowth-specific action to relieve uncontrolled and serious itching, in particular, from atopic eczema.
摘要：
膳食鞘脂例如葡萄糖神经酰胺(GlcCer)是与预防代谢综合征相关的潜在营养因素。我们目前的理解是，膳食GlcCer在肠道中降解为神经酰胺，并进一步代谢为类鞘氨醇碱。然而,神经酰胺仅在食用植物中发现痕量，因此经常在健康补充剂中用作GlcCer。在本研究中,我们使用神经酰胺糖内切酶I（EGCaseI）成功制备了魔芋神经酰胺（kCer）。魔芋,一种植物块茎，是GlcCer(kGlcCer)的丰富来源，并已作为膳食补充剂商业化，以改善由表皮神经酰胺缺乏引起的皮肤干燥和瘙痒。皮肤细胞产生的神经生长因子（NGF）是皮肤角质层中的瘙痒因子之一。已知信号素3A(Sema3A)抑制NGF诱导的表皮神经纤维的神经突生长。众所周知，瘙痒感受NGF和Sema3A之间的平衡调节。在本研究中,虽然kGlcCer对NGF诱导的PC12细胞的神经突生长没有体外抑制作用，kCer被证明可以抑制显着的神经突生长。此外,在细胞形态变化和神经突缩回方面，kCer的作用与Sema3A相似，但不同于C2-神经酰胺。KCer展示了类似Sema3A的动作，导致CRMP2磷酸化，导致神经突生长锥崩溃。因此，预计kCer是一种先进的魔芋神经酰胺材料，可能具有神经突生长特异性作用，以缓解不受控制和严重的瘙痒，特别是,特应性湿疹.
