Gu Xiangyue, Wang Botao, Zhang Tianmeng, Zhang Qiuxiang, Mao Bingyong, Tang Xin, Zhao Jianxin, Cui Shumao
State Key Laboratory of Food Science and Resources, Jiangnan University, Wuxi 214122, China.
School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
Nutrients. 2025 May 26;17(11):1803. doi: 10.3390/nu17111803.
Acne vulgaris, a prevalent inflammatory skin disorder, stems from factors like overgrowth, inflammation dysregulation, and immune dysfunction. Clinically, acne severity inversely correlates with serum zinc (Zn) levels, and oral Zn supplementation shows efficacy. Lactic acid bacteria are capable of converting inorganic Zn into organic forms via biological transformation, potentially generating Zn-enriched bacteria as superior Zn delivery vehicles. In this study, a Zn-deficient acne mouse model was established through dietary Zn restriction combined with intradermal injection. The therapeutic effects of orally administered Zn-containing supplements, including Zn-enriched subsp. CCFM1195 (Zn-CCFM1195), were systematically evaluated through multiple parameters: histopathological evaluation of skin lesions, cutaneous inflammatory and oxidative stress markers, serum Zn concentration, and gene expression levels of pathway-associated proteins. Induction of led to decreased serum Zn levels (14.98 μmol/L in Control vs. 9.71 μmol/L in Model) and skin metallothionein content, causing Zn imbalance. Zn deficiency caused increased levels of lesion elevation (9.23 in Model vs. 10.53 in Zn-deficient Model), IL-17A, TNF-α, and MMP9 in skin, thereby exacerbating the inflammatory response in C. -induced mice. Zn supplementation alleviated inflammatory responses and oxidative stress in Zn-deficient acne-like mice. Notably, inactivated Zn-CCFM1195 exhibited superior efficacy to ZnSO, significantly reducing lesion diameter and decreasing cutaneous levels of IL-1β, IL-17A, and MDA while enhancing GSH-Px activity. Similarly, viable Zn-CCFM1195 treatment significantly decreased IL-17A and enhanced GSH-Px activity compared with ZnSO treatment. Furthermore, Zn supplementation downregulated the expression of TLR2, IκBα, and IKKβ, which may exert its anti-acne effect by regulating related pathways. Zn deficiency exacerbates skin inflammation, whereas Zn supplementation, particularly with Zn-CCFM1195, alleviates acne vulgaris through anti-inflammatory and antioxidant effects.
寻常痤疮是一种常见的炎症性皮肤病，由过度生长、炎症调节异常和免疫功能障碍等因素引起。临床上，痤疮严重程度与血清锌（Zn）水平呈负相关，口服补锌显示出疗效。乳酸菌能够通过生物转化将无机锌转化为有机形式，有可能产生富含锌的细菌作为优质的锌递送载体。在本研究中，通过饮食锌限制联合皮内注射建立了缺锌痤疮小鼠模型。通过多个参数系统评估了口服含锌补充剂（包括富含锌的CCFM1195亚种（Zn-CCFM1195））的治疗效果：皮肤病变的组织病理学评估、皮肤炎症和氧化应激标志物、血清锌浓度以及通路相关蛋白的基因表达水平。诱导导致血清锌水平降低（对照组为14.98 μmol/L，模型组为9.71 μmol/L）和皮肤金属硫蛋白含量降低，导致锌失衡。锌缺乏导致皮肤病变隆起水平升高（模型组为9.23，缺锌模型组为10.53）、IL-17A、TNF-α和MMP9水平升高，从而加剧了诱导的小鼠的炎症反应。补锌减轻了缺锌痤疮样小鼠的炎症反应和氧化应激。值得注意的是，灭活的Zn-CCFM1195表现出优于ZnSO的疗效，显著减小病变直径并降低皮肤中IL-1β、IL-17A和MDA的水平，同时增强GSH-Px活性。同样，与ZnSO处理相比，活的Zn-CCFM1195处理显著降低IL-17A并增强GSH-Px活性。此外，补锌下调了TLR2、IκBα和IKKβ的表达，其可能通过调节相关通路发挥抗痤疮作用。锌缺乏会加剧皮肤炎症，而补锌，特别是使用Zn-CCFM1195，通过抗炎和抗氧化作用减轻寻常痤疮。
