紅光發光二極體對黑色素母細胞的生物效應—白斑治療的理論基礎

Abstract

在紅光與紅外光波段的發光二極體（Light emitting dioide，又簡稱 LED），一種低能量光源，已被證實在促進傷口癒合與促進視神經的傷害的恢復有功效。直到最近，紅光的發光二級體也被報告對於治療白斑有效。白斑是一種後天性，黑色素細胞的功能缺失所造成的疾病，細胞可能是經由凋亡的途徑破壞。相對於傳統的治療方式中的氦氖雷射(He-Ne laser) (632.8nm)，發光二級體可以發射類似波長，價格低廉，機器不易耗損，且單次治療時間也較短。然而白斑以發光二級體治療，截至目前為止，仍未有進一步的有關於其作用在細胞上機轉的報告。在此研究中，我們使用研究白斑常用的NCCmelb4 and NCCmelan5兩株黑色素母細胞珠來研究LED 光源對黑色素母細胞的抗凋亡的細胞保護功能，並且排除其對於細胞直接造成細胞增生，細胞移動，或黑色素增加的機轉，希望為其治療白斑的應用提供依據。 本研究發現，紅光二極體照光4J/cm2為兩株黑色素母細胞的致死量，照射1J/ cm2時，為最有效果的劑量。以1J/ cm2照光後，正常營養狀態的成熟黑色素母細胞，其黑色素含量，細胞數，總細胞活性，與移動能力皆有被抑制的情形。在不成熟的黑色素母細胞，紅光二極體的抑制狀況則不如成熟黑色素母細胞明顯。但是若在血清缺乏下，紅光二極體照射1J/ cm2可以預防黑色素母細胞的死亡，並且可以使bax/bcl-2 mRNA 表現比例減少。 結論: 我們發現紅光二極體照光治療白斑的機制，並非在於直接促進黑色素增加，使細胞增生，或是使細胞移動能力增加，反而是使黑色素母細胞一些生理功能停歇，經由調節經粒腺體的凋亡機轉，來預防黑色素母細胞的死亡，進而達到保護的作用。

Light emitting dioide (LED), in the red and infrared spectrum has proved efficacy in stimulating wound healing and accelerating optic nerve recovery. Very recently, the LED (630nm) has shown effects on repigmentation of vitiligo. Vitiligo is an acquired pigmentary disorder resulting from melanocyte destruction, which is thought to be mediated by apoptosis. Compared to low energy He-Ne laser, which is now used in treating vitiligo, LED with similar wavelength, is cheaper, longer-lasting, and requires less treatment time. However, the molecular mechanism of LED light on the activation of melanocytic cells has not been investigated. In this study, we utilized NCCmelan5 and NCCmelb4 melanoblast (MB), two melanoblast cell lines which were previously used to investigate the treatment of vitiligo, to investigate the anti-apoptotic effects of LED (630nm), and ruled out others causes of repigmentation including proliferation, mitochondrial metabolism, melanin production, migration distances of MBs after irradiation, to formulate the theoretical basis LED’s treatment of vitiligo. MBs showed 4J/cm2 to be the lethal dose and 1J/cm2 to be the effective dose for MBs. In mature MBs, there was decrement on total metabolism, cell number, melanin synthesis, and migration after irradiation, however, the effect of inhibition was not obvious for immature MBs. Under serum deprivation, pretreatment with LED (1J/cm2 ) has shown protective effect against cell death and down-regulated bax/bcl-2 mRNA expression ratio. In this study, we found that the mechanism for LED (630nm) repigmentation in vitiliginous skin is not through direct stimulation of melanin synthesis, proliferation, nor cellular migration. On the contrary, LED puts healthy MBs to arrest and prevents death of un-healthy cells through a cyto-protective mechanism with regulation of the mitochondria pathway of apoptosis.