Dermatology Department, Faculty of medicine, Cairo University, Cairo, Egypt.
Biochemistry Department, Faculty of Medicine, Cairo University, Cairo, Egypt.
Photodermatol Photoimmunol Photomed. 2021 Jul;37(4):306-312. doi: 10.1111/phpp.12653. Epub 2021 Jan 16.
Despite exhaustive research, melanocyte disappearance and the evolution of vitiligo remain enigmatic, and although multi-factorial, oxidative stress appears as a major player. The role of cutaneous cholinergic system in vitiligo pathogenesis has also been reported in some studies.
To evaluate and correlate the influence of phototherapy on cutaneous cholinergic system and oxidative stress in vitiligo.
Acetyl choline (ACh), its receptors; nicotinic (nAChR) and muscarinic (mAChR); acetylcholine esterase (AChE) and H O levels were estimated in de-pigmented and re-pigmented lesions of 30 vitiligo patients before and after NB-UVB phototherapy and in 30 controls. ACh and H O levels were measured by colorimetry. AChE and acetylcholine receptors expression were measured by quantitative real-time PCR.
Mean ACh and H O levels were significantly higher in vitiligo lesions before NB-UVB (P < .001) whereas AChE enzyme level was significantly lower (P < .001) compared to both re-pigmented and control skin. Additionally, mean mAChR was significantly higher and mean nAChR was significantly lower in vitiligo lesions before NB-UVB versus controls and re-pigmented skin (P < .001). Also, H O and AChE showed negative correlation whereas ACh and mAChR showed significant positive correlation. Although all the studied parameters showed significant changes after treatment and subsequent re-pigmentation, a significant difference continued to exist between all vitiligo skin and controls.
Cholinergic system is strongly involved in vitiligo pathogenesis through H O inhibition of AChE which could be reversed by NB-UVB. Moreover, the strong activation of mAChRs may reflect genetic and/or acquired errors, direct up-regulation by ACh and H O or both.
尽管进行了详尽的研究,但黑素细胞消失和白癜风的演变仍然是个谜,尽管是多因素的,但氧化应激似乎是一个主要因素。一些研究还报道了皮肤胆碱能系统在白癜风发病机制中的作用。
评估并关联光疗对白癜风皮肤胆碱能系统和氧化应激的影响。
在接受 NB-UVB 光疗前后,我们评估并比较了 30 名白癜风患者的去色素和再色素皮损中的乙酰胆碱(ACh)、其受体;烟碱型(nAChR)和毒蕈碱型(mAChR);乙酰胆碱酯酶(AChE)和 H O 水平,并在 30 名对照者中进行了比较。通过比色法测量 ACh 和 H O 水平。通过实时定量 PCR 测量 AChE 和乙酰胆碱受体的表达。
与再色素和对照皮肤相比,NB-UVB 前白癜风病变中的平均 ACh 和 H O 水平显著升高(P<0.001),而 AChE 酶水平显著降低(P<0.001)。此外,与对照皮肤和再色素皮肤相比,NB-UVB 前白癜风病变中的平均 mAChR 显著升高,平均 nAChR 显著降低(P<0.001)。此外,H O 和 AChE 呈负相关,而 ACh 和 mAChR 呈显著正相关。尽管所有研究参数在治疗和随后的再色素化后均显示出显著变化,但所有白癜风皮肤与对照者之间仍存在显著差异。
胆碱能系统通过抑制 AChE 的 H O 强烈参与白癜风的发病机制,而 NB-UVB 可逆转这一过程。此外,mAChRs 的强烈激活可能反映了遗传和/或获得性错误、ACh 和 H O 的直接上调或两者兼有。