油性敏感皮肤发生机制及干预护理初探

doi:10.3969/j.issn.2097-2806.2024.08.014

摘要/Abstract

摘要：

随着现代不良生活习惯的普遍发生、环境污染的加剧，油性敏感皮肤的发病率不断攀升，但确切发病机制仍未完全明晰。本文回顾了油性敏感皮肤的定义及特征，综述了其可能的发生机制，包括皮脂腺分泌过多、表皮屏障功能降低、皮肤微生态失衡、炎症反应、神经与血管高反应等，并深入分析不同发生机制之间的内在联系。针对这些机制，探讨了油性敏感皮肤的一系列干预护理建议，包括与干性敏感皮肤的护理差异、护肤品功效选择、生活习惯调整，有望改善患者的生活质量，为相关从业人员提供科学有益的参考。

关键词: 皮脂腺, 表皮屏障, 微生态, 炎症反应, 神经与血管高反应

Abstract:

With the prevalence of modern unhealthy lifestyle habits and the worsening of environmental pollution, the occurrence of oily sensitive skin has been increasing. However, the exact cause is still not completely understood. In this paper, we review the definition and characteristics of oily sensitive skin. We also provide an overview of its possible mechanisms, which include excessive sebaceous gland secretion, reduced epidermal barrier function, skin microecological imbalance, inflammatory response, and neurological and vascular hyperreactivity. Furthermore, we analyze the intrinsic connection between these different mechanisms in depth. In response to these mechanisms, this article discusses a series of recommendations for caring for oily sensitive skin. It highlights the differences in skincare compared to dry sensitive skin, emphasizes the importance of choosing effective skincare products, and suggests making adjustments to lifestyle habits. These recommendations aim to improve the quality of life for patients and provide valuable references for practitioners in the field.

Key words: sebaceous glands, epidermal barrier, microecology, inflammatory response, neurologic and vascular hyperreactivity

中图分类号:

TQ658

况昕珏,付媛媛,陈显才,陈勇,刘有停,易帆. 油性敏感皮肤发生机制及干预护理初探[J]. 日用化学工业（中英文）, 2024, 54(8): 988-996.

Xinjue Kuang,Yuanyuan Fu,Xiancai Chen,Yong Chen,Youting Liu,Fan Yi. A preliminary study on the mechanism of oily sensitive skin and intervention care[J]. China Surfactant Detergent & Cosmetics, 2024, 54(8): 988-996.

图/表 4

图1

表1

表2

油性敏感皮肤与干性敏感皮肤的差异"

皮肤类型	干性敏感皮肤	油性敏感皮肤
常见人群	常见于干燥气候、缺水、年龄较大或体质较弱的人群，可能更常见于女性	常见于青春期、荷尔蒙水平波动较大的年轻人群，无论性别都可能发生
伴随肌肤问题	1. 皮肤干燥、脱屑和紧绷感。2. 缺乏光泽和弹性，可能感觉不透气。3. 可能出现红斑、瘙痒、刺激感和灼热感等过敏症状	1. 油光和毛孔扩大。2. 容易出现青春痘、粉刺和炎症。3. 皮肤可能表现出敏感、刺激和瘙痒等症状
机理相同点	1. 干性敏感皮肤和油性敏感皮肤都可能由遗传因素、环境因素、荷尔蒙水平变化、压力和过度清洁等因素引起。2. 两者都可能与皮肤的屏障功能受损以及皮肤的天然保湿因子失调相关。3. 干性敏感皮肤和油性敏感皮肤都容易对外界刺激物和化妆品过敏
机理不同点	主要由皮肤缺水和油脂分泌不足引起干燥和敏感	主要由皮脂过多导致毛孔堵塞和炎症反应，进而引发敏感和问题皮肤
护理方案	1. 补水保湿：使用温和的、不带刺激的洁肤品和保湿产品，给皮肤提供充足的水分。2. 强化皮肤屏障：采用滋润力、封闭性更强的固体油脂，提高滋润保湿性、重构皮肤屏障、镇静舒缓，以减少水分散失。3. 避免刺激：避免使用含有刺激性成分的产品，同时注意避免过度清洁和频繁使用磨砂膏等刺激物品	1. 温和清洁：使用适合油性皮肤的温和洁面产品，帮助控制油脂分泌但不过度清洁。2. 控油祛痘：选择调理油脂分泌的产品，如含有控油成分的面霜、乳液等。使用祛痘产品靶向进行修护。3. 强化皮肤屏障：使用含有保湿成分的面霜、乳液等产品来加强皮肤屏障功能，以减少水分散失。4. 避免刺激：避免使用刺激性产品和过度揉搓皮肤，以免引起炎症和刺激反应
防晒需求	通常需要选择含有较高保湿成分的防晒产品，以避免进一步引起皮肤干燥和不适	通常需要选择质地较轻薄、不阻塞毛孔的防晒产品，以避免进一步加重皮肤油脂产生和阻塞毛孔
饮食和生活习惯	适当增加水果、蔬菜和富含健康脂肪的食物摄入，并保持合理的水分摄入	减少高油脂、高糖分和刺激性食物的摄入，控制压力和维持规律的作息时间

表2

图 2

参考文献 59

[1]	Brenaut E, Misery L, Taieb C. Sensitive skin in the indian population: An epidemiological approach[J]. Front Med (Lausanne), 2019, 6: 29.
[2]	Baumann L. Understanding and treating various skin types: The baumann skin type indicator[J]. Dermatol. Clin., 2008, 26 (3) : 359-373. doi: 10.1016/j.det.2008.03.007 pmid: 18555952
[3]	Misery L, Weisshaar E, Brenaut E, et al. Pathophysiology and management of sensitive skin: Position paper from the special interest group on sensitive skin of the international forum for the study of itch (IFSI)[J]. J. Eur. Acad. Dermatol. Venereol., 2020, 34 (2) : 222-229. doi: 10.1111/jdv.16000 pmid: 31660659
[4]	Bataille V, Snieder H, MacGregor A J, et al. The influence of genetics and environmental factors in the pathogenesis of acne: A twin study of acne in women[J]. J. Invest. Dermatol., 2002, 119 (6) : 1317-1322. doi: 10.1046/j.1523-1747.2002.19621.x pmid: 12485434
[5]	Misery L, Boussetta S, Nocera T, et al. Sensitive skin in europe[J]. J. Eur. Acad. Dermatol. Venereol., 2009, 23 (4) : 376-381. doi: 10.1111/j.1468-3083.2008.03037.x pmid: 19335729
[6]	Downing D T, Stewart M E, Wertz P W, et al. Essential fatty acids and acne[J]. J. Am. Acad. Dermatol., 1986, 14 (2 Pt 1) : 221-225. doi: 10.1016/s0190-9622(86)70025-x pmid: 2936775
[7]	Primavera G, Berardesca E. Sensitive skin: Mechanisms and diagnosis[J]. Int. J. Cosmet. Sci., 2005, 27 (1) : 1-10.
[8]	Shi V Y, Leo M, Hassoun L, et al. Role of sebaceous glands in inflammatory dermatoses[J]. J. Am. Acad. Dermatol., 2015, 73 (5) : 856-863. doi: 10.1016/j.jaad.2015.08.015 pmid: 26386632
[9]	Hong J Y, Park S J, Seo S J, et al. Oily sensitive skin: A review of management options[J]. J. Cosmet. Dermatol., 2020, 19 (5) : 1016-1020.
[10]	Roh M, Han M, Kim D, et al. Sebum output as a factor contributing to the size of facial pores[J]. Br. J. Dermatol., 2006, 155 (5) : 890-894.
[11]	Fritsch M, Orfanos C E, Zouboulis C C. Sebocytes are the key regulators of androgen homeostasis in human skin[J]. J. Invest. Dermatol., 2001, 116 (5) : 793-800. pmid: 11348472
[12]	Wilson J D, Griffin J E, Russell D W. Steroid 5 alpha-reductase 2 deficiency[J]. Endocr. Rev., 1993, 14 (5) : 577-593. doi: 10.1210/edrv-14-5-577 pmid: 8262007
[13]	Elsaie M L. Hormonal treatment of acne vulgaris: An update[J]. Clin. Cosmet. Investig. Dermatol., 2016, 9: 241-248.
[14]	Orock A, Louwies T, Ligon C O, et al. Environmental enrichment prevents stress-induced epigenetic changes in the expression of glucocorticoid receptor and corticotrophin releasing hormone in the central nucleus of the amygdala to inhibit visceral hypersensitivity[J]. Experimental Neurology, 2021, 345: 113841.
[15]	Liu Y Z, Wang Y X, Jiang C L. Inflammation: The common pathway of stress-related diseases[J]. Frontiers in Human Neuroscience, 2017, 11: 401.
[16]	Zouboulis C C. Acne and sebaceous gland function[J]. Clin. Dermatol., 2004, 22 (5) : 360-366. doi: 10.1016/j.clindermatol.2004.03.004 pmid: 15556719
[17]	Baldwin H, Tan J. Effects of diet on acne and its response to treatment[J]. Am. J. Clin. Dermatol., 2021, 22 (1) : 55-65.
[18]	Kwon G, Marshall C A, Pappan K L, et al. Signaling elements involved in the metabolic regulation of mtor by nutrients, incretins, and growth factors in islets[J]. Diabetes, 2004, 53 Suppl 3: 225-232. pmid: 15561916
[19]	Lee S H, Jeong S K, Ahn S K. An update of the defensive barrier function of skin[J]. Yonsei. Med. J., 2006, 47 (3) : 293-306. doi: 10.3349/ymj.2006.47.3.293 pmid: 16807977
[20]	Harris-Tryon T A, Grice E A. Microbiota and maintenance of skin barrier function[J]. Science, 2022, 376 (6596) : 940-945. doi: 10.1126/science.abo0693 pmid: 35617415
[21]	Fan L, He C, Jiang L, et al. Brief analysis of causes of sensitive skin and advances in evaluation of anti-allergic activity of cosmetic products[J]. Int. J. Cosmet. Sci., 2016, 38 (2) : 120-127.
[22]	Stalder J F, Tennstedt D, Deleuran M, et al. Fragility of epidermis and its consequence in dermatology[J]. J. Eur. Acad. Dermatol. Venereol., 2014, 28 Suppl 4: 1-18. doi: 10.1111/jdv.12509 pmid: 24931580
[23]	Rippke F, Schreiner V, Schwanitz H J. The acidic milieu of the horny layer: New findings on the physiology and pathophysiology of skin ph[J]. Am. J. Clin. Dermatol., 2002, 3 (4) : 261-272. pmid: 12010071
[24]	Ananthapadmanabhan K P, Moore D J, Subramanyan K, et al. Cleansing without compromise: The impact of cleansers on the skin barrier and the technology of mild cleansing[J]. Dermatol. Ther., 2004, 17 Suppl 1: 16-25. pmid: 14728695
[25]	Schommer N N, Gallo R L. Structure and function of the human skin microbiome[J]. Trends Microbiol., 2013, 21 (12) : 660-668. doi: 10.1016/j.tim.2013.10.001 pmid: 24238601
[26]	Nakatsuji T, Chen T H, Narala S, et al. Antimicrobials from human skin commensal bacteria protect against staphylococcus aureus and are deficient in atopic dermatitis[J]. Sci. Transl. Med., 2017, 9 (378) : eaah4680.
[27]	Delanghe L, Spacova I, Van Malderen J, et al. The role of lactobacilli in inhibiting skin pathogens[J]. Biochem. Soc. Trans., 2021, 49 (2) : 617-627.
[28]	Brüggemann H, Henne A, Hoster F, et al. The complete genome sequence of propionibacterium acnes, a commensal of human skin[J]. Science, 2004, 305 (5684) : 671-673. pmid: 15286373
[29]	Park M, Park S, Jung W H. Skin commensal fungus malassezia and its lipases[J]. J. Microbiol. Biotechnol., 2021, 31 (5) : 637-644.
[30]	Iebba V, Totino V, Gagliardi A, et al. Eubiosis and dysbiosis: The two sides of the microbiota[J]. New Microbiol., 2016, 39 (1) : 1-12. pmid: 26922981
[31]	Barker J N, Mitra R S, Griffiths C E, et al. Keratinocytes as initiators of inflammation[J]. Lancet, 1991, 337 (8735) : 211-214. doi: 10.1016/0140-6736(91)92168-2 pmid: 1670850
[32]	Carmina E, Godwin A J, Stanczyk F Z, et al. The association of serum androsterone glucuronide with inflammatory lesions in women with adult acne[J]. J. Endocrinol. Invest., 2002, 25 (9) : 765-768. pmid: 12398233
[33]	Turner M D, Nedjai B, Hurst T, et al. Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease[J]. Biochim. Biophys. Acta., 2014, 1843 (11) : 2563-2582. doi: S0167-4889(14)00196-7 pmid: 24892271
[34]	Schindler R, Mancilla J, Endres S, et al. Correlations and interactions in the production of interleukin-6 (IL-6), IL-1, and tumor necrosis factor (TNF) in human blood mononuclear cells: IL-6 suppresses IL-1 and TNF[J]. Blood, 1990, 75 (1) : 40-47. pmid: 2294996
[35]	Lawrence T, Willoughby D A, Gilroy D W. Anti-inflammatory lipid mediators and insights into the resolution of inflammation[J]. Nat. Rev. Immunol., 2002, 2 (10) : 787-795. doi: 10.1038/nri915 pmid: 12360216
[36]	Koohgoli R, Hudson L, Naidoo K, et al. Bad air gets under your skin[J]. Exp. Dermatol., 2017, 26 (5) : 384-387. doi: 10.1111/exd.13257 pmid: 27892609
[37]	Lee C W, Lin Z C, Hu S C, et al. Urban particulate matter down-regulates filaggrin via COX2 expression/PGE2 production leading to skin barrier dysfunction[J]. Sci. Rep., 2016, 6: 27995.
[38]	Sklar L R, Almutawa F, Lim H W, et al. Effects of ultraviolet radiation, visible light, and infrared radiation on erythema and pigmentation: A review[J]. Photochem. Photobiol. Sci., 2013, 12 (1) : 54-64.
[39]	Eming S A, Hubbell J A. Extracellular matrix in angiogenesis: Dynamic structures with translational potential[J]. Exp. Dermatol., 2011, 20 (7) : 605-613. doi: 10.1111/j.1600-0625.2011.01309.x pmid: 21692861
[40]	Roosterman D, Goerge T, Schneider S W, et al. Neuronal control of skin function: The skin as a neuroimmunoendocrine organ[J]. Physiol. Rev., 2006, 86 (4) : 1309-1379. doi: 10.1152/physrev.00026.2005 pmid: 17015491
[41]	Laverdet B, Danigo A, Girard D, et al. Skin innervation: Important roles during normal and pathological cutaneous repair[J]. Histol. Histopathol., 2015, 30 (8) : 875-892. doi: 10.14670/HH-11-610 pmid: 25799052
[42]	Yosipovitch G, Misery L, Proksch E, et al. Skin barrier damage and itch: Review of mechanisms, topical management and future directions[J]. Acta. Derm. Venereol., 2019, 99 (13) : 1201-1209.
[43]	Kueper T, Krohn M, Haustedt L O, et al. Inhibition of TRPV1 for the treatment of sensitive skin[J]. Exp. Dermatol., 2010, 19 (11) : 980-986. doi: 10.1111/j.1600-0625.2010.01122.x pmid: 20626462
[44]	Darré L, Domene C. Binding of capsaicin to the TRPV1 ion channel[J]. Mol. Pharm., 2015, 12 (12) : 4454-4465.
[45]	Weiss E, Katta R. Diet and rosacea: The role of dietary change in the management of rosacea[J]. Dermatol. Pract. Concept., 2017, 7 (4) : 31-37. doi: 10.5826/dpc.0704a08 pmid: 29214107
[46]	O’Donohue T L, Chronwall B M, Pruss R M, et al. Neuropeptide Y and peptide YY neuronal and endocrine systems[J]. Peptides, 1985, 6 (4) : 755-768. pmid: 3906595
[47]	Herbert M K, Holzer P. Neurogenic inflammation. I. Basic mechanisms, physiology and pharmacology[J]. Anasthesiol Intensivmed Notfallmed Schmerzther, 2002, 37 (6) : 314-325.
[48]	Jiang W C, Zhang H, Xu Y, et al. Cutaneous vessel features of sensitive skin and its underlying functions[J]. Skin Res. Technol., 2020, 26 (3) : 431-437.
[49]	Sprague A H, Khalil R A. Inflammatory cytokines in vascular dysfunction and vascular disease[J]. Biochem. Pharmacol., 2009, 78 (6) : 539-552. doi: 10.1016/j.bcp.2009.04.029 pmid: 19413999
[50]	Hebert A A, Kwong C W, Neri I. Promoting integrated care in eczematous dermatitis and dry sensitive skin[J]. Skinmed, 2022, 20 (6) : 414-419.
[51]	Draelos Z D. New treatments for restoring impaired epidermal barrier permeability: Skin barrier repair creams[J]. Clin. Dermatol., 2012, 30 (3) : 345-348. doi: 10.1016/j.clindermatol.2011.08.018 pmid: 22507050
[52]	Man M M, Feingold K R, Thornfeldt C R, et al. Optimization of physiological lipid mixtures for barrier repair[J]. J. Invest. Dermatol., 1996, 106 (5) : 1096-1101. pmid: 8618046
[53]	Ishikawa J, Shimotoyodome Y, Chen S, et al. Eucalyptus increases ceramide levels in keratinocytes and improves stratum corneum function[J]. Int. J. Cosmet. Sci., 2012, 34 (1) : 17-22.
[54]	Li H E. Effects of prinsepia utilis royle oil on the synthesis of ceramide and expression of ceramidase[J]. Prinsepia Utilis Royle Oil, 2012, 45 (10) : 718-722.
[55]	Anggraeni S, Umborowati M A, Damayanti D, et al. Role of centella asiatica and ceramide in skin barrier improvement: A double blind clinical trial of indonesian batik workers[J]. J. Basic. Clin. Physiol. Pharmacol., 2021, 32 (4) : 589-593. doi: 10.1515/jbcpp-2020-0510 pmid: 34214362
[56]	Chandrashekhar V M, Halagali K S, Nidavani R B, et al. Anti-allergic activity of german chamomile (Matricaria recutita L.) in mast cell mediated allergy model[J]. J. Ethnopharmacol., 2011, 137 (1) : 336-340. doi: 10.1016/j.jep.2011.05.029 pmid: 21651969
[57]	Elias P M. Optimizing emollient therapy for skin barrier repair in atopic dermatitis[J]. Ann. Allergy Asthma Immunol., 2022, 128 (5) : 505-511.
[58]	Yang J, Shi L, Xu D, et al. 5-aminolaevulinic acid photodynamic therapy suppresses lipid secretion of primary sebocytes through AMPK/SREBP-1 pathway[J]. Photodiagnosis. Photodyn. Ther., 2021, 36: 102537.
[59]	Gupta M, Singh N, Gulati M, et al. Herbal bioactives in treatment of inflammation: An overview[J]. South African Journal of Botany, 2021, 143: 205-225.

发生机理	描述	相互作用/相互影响
激素水平与皮脂	雄激素可刺激皮脂腺过度分泌油脂，内源性激素（如雄激素、孕激素）对油脂分泌的调节	激素分泌受到饮食、压力等因素的影响
炎症与神经、血管高反应	油脂过量、毛孔堵塞可引发炎症反应、刺激神经和血管高反应；炎症反应可引发红肿、瘙痒等敏感症状，受血管高反应影响	炎症反应和血管高反应可能加重油脂分泌，并受神经调节影响，可受外界刺激和炎症反应的影响，加重敏感症状
皮脂与微生态	皮脂腺分泌油脂过多，导致皮肤微生物群落不平衡，微生态失衡	可导致炎症反应、加重皮肤屏障受损，可被外界刺激和激素影响增加
皮脂与皮肤屏障	适度皮脂参与形成皮肤屏障，保护皮肤，过度则导致皮肤屏障功能受到破坏，易受外界刺激	可加重皮肤对刺激物的敏感度，引发炎症反应
其他因素	行为因素（如饮食、压力、生活习惯、化妆品使用等）、外界环境因素（如气候、污染物、紫外线等）对皮肤的刺激作用，可能影响油脂分泌和炎症反应	可能加重油脂分泌和炎症反应，而油脂分泌又可能受到这些因素的调节，加重外界刺激、干扰皮肤微生态、引发血管高反应