research-focus Research Focus International Scientific Journal Research Focus 2181-3833 Ilm-fan va innovatsiyalar akademiyasi 10.66073/researchfocus.v4i11.1870 REL-A-013186 14.00.00 ВЛИЯНИЕ ОКСИДАТИВНОГО СТРЕССА И МИТОХОНДРИАЛЬНОЙ ДИСФУНКЦИИ НА РАЗВИТИЕ ВОСПАЛИТЕЛЬНЫХ ФОРМ АКНЕ THE INFLUENCE OF OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION ON THE DEVELOPMENT OF INFLAMMATORY FORMS OF ACNE OKSIDATIV STRESS VA MITOXONDRIAL DISFUNKSIYANING AKNENING YALLIG‘LANISHLI SHAKLLARI RIVOJLANISHIGA TA‘SIRI Баротова Мавжуда Раимовна Самаркандский государственный медицинский университет. Узбекистан, г. Самарканд, ул. Амира Темура, 18. 05 12 2025 2025 4 11 299 305 https://creativecommons.org/licenses/by/4.0 Это произведение доступно по лицензии Creative Commons «Attribution» («Атрибуция») 4.0 Всемирная.

в данном исследовании проведена комплексная оценка роли оксидативного стресса и митохондриальной дисфункции в патогенезе воспалительных форм акне с целью установления их связи с клинической тяжестью заболевания. Анализ проводился путём сравнения показателей пациентов с контрольной группой здоровых добровольцев. На основании клинических и лабораторных данных определены степень выраженности оксидативного стресса, характер митохондриальной дисфункции и профиль провоспалительных цитокинов. Интенсивность липопероксидации, активность антиоксидантной системы и параметры митохондриальной функции были проанализированы с использованием корреляционного анализа. Кроме того, для клинических проявлений акне рассчитаны корреляции с лабораторными маркерами, что является важным прогностическим и патогенетическим показателем.

This study presents a comprehensive assessment of the role of oxidative stress and mitochondrial dysfunction in the pathogenesis of inflammatory forms of acne in order to establish their relationship with the clinical severity of the disease. The analysis was carried out by comparing the indicators of the patients with a control group of healthy volunteers. On the basis of clinical and laboratory data, the severity of oxidative stress, the nature of mitochondrial dysfunction and the profile of pro-inflammatory cytokines were determined. The intensity of lipid peroxidation, the activity of the antioxidant system and the parameters of mitochondrial function were analysed using correlation analysis. In addition, correlations of the clinical manifestations of acne with laboratory markers were calculated, which is an important prognostic and pathogenetic indicator.

Ushbu tadqiqotda oksidativ stress va mitoxondrial disfunksiyaning aknening yallig‘lanishli shakllari patogenezidagi roli kompleks baholanib, ularning kasallikning klinik og‘irligi bilan bog‘liqligini aniqlash ko‘zda tutilgan. Tahlil bemorlar ko‘rsatkichlarini sog‘lom ko‘ngillilardan iborat nazorat guruhi bilan taqqoslash yo‘li bilan o‘tkazildi. Klinik va laboratoriya ma‘lumotlari asosida oksidativ stressning ifodalanish darajasi, mitoxondrial disfunksiyaning xarakteri va proyallig‘lanish sitokinlari profili aniqlandi. Lipoperoksidatsiya jadalligi, antioksidant tizim faolligi va mitoxondriya funksiyasi parametrlari korrelyatsion tahlil yordamida o‘rganildi. Bundan tashqari, aknening klinik ko‘rinishlari uchun laboratoriya markerlari bilan korrelyatsiyalar hisoblab chiqildi, bu esa muhim prognostik va patogenetik ko‘rsatkichdir.

 акне vulgaris оксидативный стресс митохондриальная дисфункция ΔΨm NLRP3-инфламмасома малоновый диальдегид антиоксидантные ферменты IL-1β IL-8 TNF-α. acne vulgaris oxidative stress mitochondrial dysfunction ΔΨm NLRP3 inflammasome malondialdehyde antioxidant enzymes IL-1β IL-8 TNF-α akne vulgaris oksidativ stress mitoxondrial disfunksiya ΔΨm NLRP3-inflammasoma malon dialdegid antioksidant fermentlar IL-1β IL-8 TNF-α Bhate K, Williams HC. Epidemiology of acne vulgaris. Br J Dermatol. 2013;168(3):474–485. Tan JK, Bhate K. A global perspective on the epidemiology of acne. Br J Dermatol. 2015;172(S1):3–12. Collier CN, et al. The prevalence of acne in adults 20 years and older. J Am Acad Dermatol. 2008;58(1):56–59. Hay RJ, et al. Global burden of skin disease. J Invest Dermatol. 2014;134(6):1527–1534. Dreno B, et al. Acne as an inflammatory disease. J Eur Acad Dermatol Venereol. 2015;29(S1):3–16. Kurokawa I, et al. New developments in our understanding of acne pathogenesis. J Dermatol. 2009;36(1):1–7. Nakatsuji T, et al. The microbiome and acne vulgaris. Semin Cutan Med Surg. 2016;35(3):108–114. Briganti S, Picardo M. Antioxidant activity, lipid peroxidation and skin diseases. Front Biosci. 2003;8:s1100–s1107. Arican O, et al. Oxidative stress in acne vulgaris. J Eur Acad Dermatol Venereol. 2005;19(4):435–439. Ozturk P, et al. Increased oxidative stress in acne vulgaris. J Clin Lab Anal. 2013;27(2):134– Sivayoganathan S, et al. Biomarkers of oxidative stress in dermatological disorders. Free Radic Biol Med. 2021;176:181–195. Bowe WP, et al. Nitric oxide and inflammatory acne. J Invest Dermatol. 2011;131(2):322– El-Akawi Z, et al. Serum copper, zinc, and lipid peroxidation in acne patients. Clin Exp Dermatol. 2006;31(6):676–680. Kurutas EB. The importance of antioxidants in acne. Arch Dermatol Res. 2015;307(9):781– Zouboulis CC, et al. The human sebocyte: A model for studying sebaceous gland differentiation and lipid metabolism. J Invest Dermatol. 1999;113(6):946–956. Kistowska M, et al. IL-1β from Cutibacterium acnes–stimulated keratinocytes triggers chronic inflammation. Nat Commun. 2014;5:5687. Törmä H, et al. Sebocytes and oxidative stress. Dermatoendocrinol. 2017;9(1):e1375638. Ottaviani M, et al. Sebum lipids and inflammation in acne. Exp Dermatol. 2010;19(12): e931– e936. Picardo M, et al. Lipid oxidation as a key event in acne. Dermatoendocrinol. 2009;1(2):68– Fitz-Gibbon S, et al. Propionibacterium acnes strain diversity. J Invest Dermatol. 2013;133(9):2152–2160. O’Neill AM, Gallo RL. Host–microbiome interactions in acne. Semin Cutan Med Surg. 2017;36(2):80–83. Jahns AC, et al. Microbial dysbiosis and acne. Front Microbiol. 2014;5:567. Lomholt HB, Kilian M. Population structure of Propionibacterium acnes. PLoS One. 2010;5(8):e12277. Mills EL, et al. Mitochondria as signaling organelles in inflammation. Cell. 2017;168(6):1228–1242. Chen Y, et al. Mitochondrial ROS and NLRP3 inflammasome activation. J Immunol. 2018;200(6):2046–2055. Weinberg SE, Sena LA, Chandel NS. Mitochondria in health and disease. Physiol Rev. 2015;95(1):219–245. West AP. Mitochondrial DNA signaling in inflammation. Nature. 2015;520:553–559. Jash S, et al. Mitochondrial dysfunction in sebocytes promotes inflammation. Free Radic Biol Med. 2020;160:10–21. Gao L, et al. Bax/Bcl-2 pathway in acne-related sebocyte apoptosis. Exp Dermatol. 2019;28(3):319–325. Melnik BC. The role of IGF-1 and mTORC1 in acne pathogenesis. Dermatoendocrinol. 2012;4(1):20–32. O’Neill CA, et al. Metabolic factors and acne inflammation. Exp Dermatol. 2020;29(12):1154–1162. Burris J, et al. Insulin resistance and acne: Mechanistic insights. J Am Acad Dermatol. 2017;76(4):627–633.