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Article(id=1250834198244831962, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1250834186500784538, articleNumber=null, orderNo=null, doi=10.13343/j.cnki.wsxb.20260111, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1770220800000, receivedDateStr=2026-02-05, revisedDate=null, revisedDateStr=null, acceptedDate=1772467200000, acceptedDateStr=2026-03-03, onlineDate=1776151712237, onlineDateStr=2026-04-14, pubDate=1775232000000, pubDateStr=2026-04-04, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1776151712237, onlineIssueDateStr=2026-04-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1776151712237, creator=13701087609, updateTime=1776151712237, updator=13701087609, issue=Issue{id=1250834186500784538, tenantId=1146029695717560320, journalId=1192105938417971205, year='2026', volume='66', issue='4', pageStart='1471', pageEnd='2021', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1776151709437, creator=13701087609, updateTime=1776152261216, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1250836500921922256, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1250834186500784538, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1250836500926116561, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1250834186500784538, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1941, endPage=1955, ext={EN=ArticleExt(id=1250834198844617475, articleId=1250834198244831962, tenantId=1146029695717560320, journalId=1192105938417971205, language=EN, title=Lacticaseibacillus paracasei CCFM1224 postbiotics alleviate sebum metabolism disorders by regulating lipid metabolism, columnId=1192149543992045670, journalTitle=Acta Microbiologica Sinica, columnName=Research Article, runingTitle=null, highlight=null, articleAbstract=

Objective Sebum metabolism disorders are a key contributing factor to various dermatological conditions. As an emerging class of microbial agents, postbiotics show potential in regulating metabolic processes. This study aimed to investigate the efficacy and mechanisms of Lacticaseibacillus paracasei CCFM1224 postbiotics in alleviating sebum metabolism disorders and explore the active components responsible for the effects. Methods Using a mouse model of oleic acid-induced sebum metabolism disorders, we comprehensively evaluated the efficacy of CCFM1224 postbiotics in ameliorating sebum imbalance. This evaluation encompassed phenotypic measurements, hormonal parameters, and skin lipid content. Changes in the expression of genes related to skin lipid metabolism were measured via real-time quantitative PCR. Subsequently, a free fatty acid-induced lipid accumulation model in HepG2 cells was utilized to screen the active components of postbiotics. Results CCFM1224 postbiotics significantly ameliorated sebum metabolism disorders in mice. This was evidenced by mitigated abnormal weight gain, a reduced testicle index, alleviated histopathological skin damage, and decreased levels of inflammatory cytokines (IL-6, IL-1β, and TNF-α) as well as triglyceride (TG) and non-esterified fatty acid (NEFA) in the skin tissue. CCFM1224 postbiotics modulated sebum metabolism by downregulating the expression of lipogenesis-related genes (FASN, PPAR-γ, and SREBP-1c) and upregulating the expression of lipolysis-related genes (PPAR-α, HSL, and ATGL). Further cellular validation identified the inactivated bacterial cell component as the key functional fraction, which effectively alleviated intracellular lipid accumulation and associated damage, thereby clarifying the material basis for the effects of CCFM1224 postbiotics. Conclusion L. paracasei CCFM1224 ameliorate sebum metabolism disorders by modulating hormone secretion and lipid metabolic pathways. The key bioactive components were identified as the inactivated bacterial cells, rather than the fermentation supernatant. This finding provides a theoretical foundation for the application of postbiotics in regulating lipid metabolism disorders and establishes a basis for developing related functional microbial preparations.

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E-mail:
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目的 皮脂代谢紊乱是多种皮肤疾病的重要诱因，后生元作为一种新兴的微生态制剂显示出调控代谢的潜力。本研究旨在探究副干酪乳酪杆菌CCFM1224后生元对皮脂代谢紊乱的改善作用及其机制，并进一步探索后生元起效组分。 方法 通过构建油酸诱导的小鼠皮脂代谢紊乱模型，从表观指标、激素指标、皮肤脂质含量水平综合评价CCFM1224后生元对皮脂紊乱的改善效果，并检测皮肤脂质代谢相关基因表达变化。利用游离脂肪酸诱导的HepG2细胞脂质堆积模型对后生元功效组分进行筛选。 结果 CCFM1224后生元能显著缓解小鼠皮脂代谢紊乱导致的体重异常增长与睾丸系数增大，减轻皮肤组织病理损伤，降低炎症因子IL-6、IL-1β和TNF-α水平，并下调皮肤组织中甘油三酯(triglyceride, TG)及游离脂肪酸(non-esterified fatty acid, NEFA)含量。机制研究表明，CCFM1224后生元通过抑制脂质合成基因(FASN、PPAR-γ、SREBP-1c)的表达，促进脂质分解基因(PPAR-α、HSL、ATGL)的表达，从而调节皮脂代谢。细胞实验表明，CCFM1224后生元灭活菌体成分能够显著减轻细胞脂质积累及相关损伤，说明其为CCFM1224后生元发挥功效的主要活性组分。 结论 副干酪乳酪杆菌CCFM1224能够通过调节激素分泌以及脂质代谢途径缓解皮脂代谢紊乱，其关键功效物质为灭活菌体组分而非发酵上清液。本研究为后生元在脂质代谢紊乱调控中的应用提供了理论依据，也为相关功能性微生物制剂的开发奠定了研究基础。

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作者贡献声明

卢勇莉：数据整理与分析、文章撰写与修改；唐鑫：实验设计、文章修改与定稿；潘正浩：数据分析；刘飞、张秋香：文章修改；毛丙永：参与文章讨论；王伯韬、石海宁：提供技术支持；赵建新：提供资源；陈卫：提供资源；崔树茂：稿件审阅。

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Food Research International, 2022, 157: 111445., articleTitle=Effects of kefir lactic acid bacteria-derived postbiotic components on high fat diet-induced gut microbiota and obesity, refAbstract=null)], funds=null, companyList=[AuthorCompany(id=1250879407259337513, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, xref=1., ext=[AuthorCompanyExt(id=1250879407309669166, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, companyId=1250879407259337513, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=1.School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu, China), AuthorCompanyExt(id=1250879407360000822, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, companyId=1250879407259337513, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=1.江南大学 食品学院，江苏 无锡)]), AuthorCompany(id=1250879407464858432, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, xref=2., ext=[AuthorCompanyExt(id=1250879407531967303, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, companyId=1250879407464858432, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=2.Bloomage Biotechnology Co. , Ltd. , Jinan, Shandong, China), AuthorCompanyExt(id=1250879407544550217, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, companyId=1250879407464858432, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=2.华熙生物科技股份有限公司，山东 济南)])], figs=[ArticleFig(id=1250879415786357209, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 1, caption=Effect of CCFM1224 postbiotics on body weight and testis coefficient in mice. A: Body weight gain; B: Testicle coefficient. **P<0.01, ***P<0.001 vs. the Model group., figureFileSmall=U/TEFbDT6mUCbzTS4xWG8Q==, figureFileBig=PQCAbugRZxrdhPECOWMt3w==, tableContent=null), ArticleFig(id=1250879415966712295, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图1, caption=CCFM1224后生元对小鼠体重和睾丸系数的影响, figureFileSmall=U/TEFbDT6mUCbzTS4xWG8Q==, figureFileBig=PQCAbugRZxrdhPECOWMt3w==, tableContent=null), ArticleFig(id=1250879416209981940, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 2, caption=Effects of CCFM1224 postbiotics on histopathological features and inflammation in mouse skin tissue. A: H&E staining of mouse skin tissue; B: IL-6 content in mouse skin tissue; C: IL-1β content in mouse skin tissue; D: TNF-α content in mouse skin tissue. IL-6: Interleukin-6; IL-1β: Interleukin-1β; TNF-α: Tumor necrosis factor-α. **P<0.01, ***P<0.001 vs. the Model group., figureFileSmall=ukWND7xmhZLsHgLHPw+IgA==, figureFileBig=su5n115NpoXjXNIg20Rq8Q==, tableContent=null), ArticleFig(id=1250879416365171200, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图2, caption=CCFM1224后生元对小鼠皮肤组织病理形态及炎症的影响, figureFileSmall=ukWND7xmhZLsHgLHPw+IgA==, figureFileBig=su5n115NpoXjXNIg20Rq8Q==, tableContent=null), ArticleFig(id=1250879416545526281, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 3, caption=Effects of CCFM1224 postbiotics on skin lipid content in mice. A: TG level in mouse skin tissue; B: NEFA level in mouse skin tissue. TG: Triglyceride; TC: Total cholesterol; NEFA: Non-esterified fatty acid. **P<0.01; ***P<0.001 vs. the Model group., figureFileSmall=wERpDiJvJweS270JAl0p/g==, figureFileBig=YwYHsEYfrTV9fOScU8EfIg==, tableContent=null), ArticleFig(id=1250879416654578192, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图3, caption=CCFM1224后生元对小鼠皮肤脂质含量的影响, figureFileSmall=wERpDiJvJweS270JAl0p/g==, figureFileBig=YwYHsEYfrTV9fOScU8EfIg==, tableContent=null), ArticleFig(id=1250879416801378841, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 4, caption=Effects of CCFM1224 postbiotics on serum hormone secretion in mice. A: Concentrations of serum testosterone; B: Concentrations of serum insulin. **P<0.01, ***P<0.001 vs. the Model group., figureFileSmall=EW6Tu7dtS/tZNgw8d/WG0w==, figureFileBig=7GKhfhOMv7kfm9HjTNqqww==, tableContent=null), ArticleFig(id=1250879416994316839, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图4, caption=CCFM1224后生元对小鼠血清激素分泌的影响, figureFileSmall=EW6Tu7dtS/tZNgw8d/WG0w==, figureFileBig=7GKhfhOMv7kfm9HjTNqqww==, tableContent=null), ArticleFig(id=1250879417241780790, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 5, caption=Effects of CCFM1224 postbiotics on lipid metabolism of skin in mice. A: Relative FASN mRNA expression; B: Relative PPAR-γ mRNA expression; C: Relative SREBP-1c mRNA expression; D: Relative PPAR-α mRNA expression; E: Relative HSL mRNA expression; F: Relative ATGL mRNA expression. FASN: Fatty acid synthase; PPAR-γ: Peroxisome-proliferator-activated receptor γ; SREBP-1c: Sterol regulatory element-binding protein 1c; PPAR-α: Peroxisome proliferator-activated receptor α; HSL: Hormone-sensitive lipase; ATGL: Adipose triglyceride lipase. *P<0.05, ***P<0.001 vs. the Model group., figureFileSmall=Z38cV75U6s+OMDAXM77+fg==, figureFileBig=pGJ/q2WHoxHS8RoNWt2D5w==, tableContent=null), ArticleFig(id=1250879417355027006, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图5, caption=CCFM1224后生元对小鼠皮肤脂质代谢的影响, figureFileSmall=Z38cV75U6s+OMDAXM77+fg==, figureFileBig=pGJ/q2WHoxHS8RoNWt2D5w==, tableContent=null), ArticleFig(id=1250879417497633354, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 6, caption=Effect of different concentrations of postbiotics components on the activity in HepG2 cells. A: Effect of CCFM1224-FS concentration on cell viability; B: Effect of CCFM1224-IB concentration on cell viability. **P<0.01, ***P<0.001 vs. the Model group., figureFileSmall=7MgKvg1s2EdCCBpyirDXsw==, figureFileBig=nCzTcMMaWxnmHZzNxyEVhA==, tableContent=null), ArticleFig(id=1250879417791234650, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图6, caption=不同浓度后生元成分对HepG2细胞活性的影响, figureFileSmall=7MgKvg1s2EdCCBpyirDXsw==, figureFileBig=nCzTcMMaWxnmHZzNxyEVhA==, tableContent=null), ArticleFig(id=1250879417912869474, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 7, caption=Effect of different concentrations of postbiotics components on the activity lipid deposition and cell damage in HepG2 cells. A: TG content; B: TC content; C: ALT content; D: AST content. TG: Triglyceride; TC: Total cholesterol; ALT: Alanine aminotransferase; AST: Aspartate aminotransferase. ***P<0.001 vs. the Model group., figureFileSmall=c3dVn/Cw+8WfnxxVIUtkWw==, figureFileBig=tMk/Ujj56gbr27g9K0UDWw==, tableContent=null), ArticleFig(id=1250879418068058733, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图7, caption=不同后生元成分对HepG2细胞脂质沉积和细胞损伤的影响, figureFileSmall=c3dVn/Cw+8WfnxxVIUtkWw==, figureFileBig=tMk/Ujj56gbr27g9K0UDWw==, tableContent=null), ArticleFig(id=1250879418193887862, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 8, caption=Effects of different concentrations of postbiotics components on lipid metabolism in HepG2 cells. A: Relative PPAR-γ mRNA expression; B: Relative SREBP-1c mRNA expression; C: Relative FASN mRNA expression; D: Relative PPAR-α mRNA expression; E: Relative CPT1 mRNA expression; F: Relative ACOX1 mRNA expression. PPAR-γ: Peroxisome-proliferator-activated receptor γ; SREBP-1c: Sterol regulatory element-binding protein 1c; FASN: Fatty acid synthase; PPAR-α: Peroxisome proliferator-activated receptor α; CPT1: Carnitine palmitoyltransferase; ACOX1: Acyl-CoA oxidase 1. *P<0.05, **P<0.01, ***P<0.001 vs. the Model group., figureFileSmall=dEzXJrLmZVhWbrol/faY3A==, figureFileBig=MtgQwHVgNuRh4TtPwDPBUw==, tableContent=null), ArticleFig(id=1250879418319716995, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图8, caption=不同后生元成分对HepG2细胞脂质代谢的影响, figureFileSmall=dEzXJrLmZVhWbrol/faY3A==, figureFileBig=MtgQwHVgNuRh4TtPwDPBUw==, tableContent=null), ArticleFig(id=1250879418470711954, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Figure 9, caption=Schematic diagram of CCFM1224 postbiotics regulating sebum metabolism disorders. IL-1β: Interleukin-1β; IL-6: Interleukin-6; TNF-α: Tumor necrosis factor-α; PPAR-γ: Peroxisome-proliferator-activated receptor γ; SREBP-1c: Sterol regulatory element-binding protein 1c; FASN: Fatty acid synthase; PPAR-α: Peroxisome proliferator-activated receptor α; HSL: Hormone-sensitive lipase; ATGL: Adipose triglyceride lipase., figureFileSmall=DzqwtacH4pjttF6ZucolDw==, figureFileBig=Hj32L4DTVf+yz5JE1eIy2A==, tableContent=null), ArticleFig(id=1250879418718175907, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=图9, caption=CCFM1224后生元调节皮脂代谢紊乱机制示意图, figureFileSmall=DzqwtacH4pjttF6ZucolDw==, figureFileBig=Hj32L4DTVf+yz5JE1eIy2A==, tableContent=null), ArticleFig(id=1250879418923696811, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Table 1, caption=

Animal experimental design

, figureFileSmall=null, figureFileBig=null, tableContent=
GroupAbbreviationOral gavage
Control groupControl0.2 mL saline
Model groupModel0.2 mL saline
Medium groupMedium0.2 mL saline+800 mg/kg medium
CCFM1224 postbiotics groupCCFM12240.2 mL saline+800 mg/kg postbiotics
), ArticleFig(id=1250879419015971505, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=表1, caption=

动物实验方案

, figureFileSmall=null, figureFileBig=null, tableContent=
GroupAbbreviationOral gavage
Control groupControl0.2 mL saline
Model groupModel0.2 mL saline
Medium groupMedium0.2 mL saline+800 mg/kg medium
CCFM1224 postbiotics groupCCFM12240.2 mL saline+800 mg/kg postbiotics
), ArticleFig(id=1250879419208909500, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Table 2, caption=

Primer sequences used for animal experiments

, figureFileSmall=null, figureFileBig=null, tableContent=
Primer namesPrimer sequences (5′→3′)
GAPDHF: AGAAGGTGGTGAAGCAGGCATC
R: CGAAGGTGGAAGAGTGGGAGTTG
PPAR-γF: TCGCTGATGCACTGCCTATG
R: GAGAGGTCCACAGAGCTGATT
SREBP-1cF: TGACCCGGCTATTCCGTGA
R: CTGGGCTGAGCAATACAGTTC
FASNF: GGAGGTGGTGATAGCCGGTAT
R: TGGGTAATCCATAGAGCCCAG
PPAR-αF: AGAGCCCCATCTGTCCTCTC
R: ACTGGTAGTCTGCAAAACCAAA
ATGLF: GGATGGCGGCATTTCAGACA
R: CAAAGGGTTGGGTTGGTTCAG
HSLF: CCAGCCTGAGGGCTTACTG
R: CTCCATTGACTGTGACATCTCG
), ArticleFig(id=1250879419477344964, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=表2, caption=

动物实验所用引物序列

, figureFileSmall=null, figureFileBig=null, tableContent=
Primer namesPrimer sequences (5′→3′)
GAPDHF: AGAAGGTGGTGAAGCAGGCATC
R: CGAAGGTGGAAGAGTGGGAGTTG
PPAR-γF: TCGCTGATGCACTGCCTATG
R: GAGAGGTCCACAGAGCTGATT
SREBP-1cF: TGACCCGGCTATTCCGTGA
R: CTGGGCTGAGCAATACAGTTC
FASNF: GGAGGTGGTGATAGCCGGTAT
R: TGGGTAATCCATAGAGCCCAG
PPAR-αF: AGAGCCCCATCTGTCCTCTC
R: ACTGGTAGTCTGCAAAACCAAA
ATGLF: GGATGGCGGCATTTCAGACA
R: CAAAGGGTTGGGTTGGTTCAG
HSLF: CCAGCCTGAGGGCTTACTG
R: CTCCATTGACTGTGACATCTCG
), ArticleFig(id=1250879419682865870, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=EN, label=Table 3, caption=

Primer sequences used for cell experiments

, figureFileSmall=null, figureFileBig=null, tableContent=
Primer namesPrimer sequences (5′→3′)
GAPDHF: CTGGGCTACACTGAGCACC
R: AAGTGGTCGTTGAGGGCAATG
PPAR-γF: GGGATCAGCTCCGTGGATCT
R: TGCACTTTGGTACTCTTGAAGTT
SREBP-1cF: GCCCCTGTAACGACCACTG
R: CAGCGAGTCTGCCTTGATG
FASNF: AAGGACCTGTCTAGGTTTGATGC
R: TGGCTTCATAGGTGACTTCCA
PPAR-αF: ATGGTGGACACGGAAAGCC
R: CGATGGATTGCGAAATCTCTTGG
CPT1F: ATCAATCGGACTCTGGAAACGG
R: TCAGGGAGTAGCGCATGGT
ACOX1F: AATCGGGACCCATAAGCCTTT
R: GGGAATACGATGGTTGTCCATTT
), ArticleFig(id=1250879419871609569, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1250834198244831962, language=CN, label=表3, caption=

细胞实验所用引物序列

, figureFileSmall=null, figureFileBig=null, tableContent=
Primer namesPrimer sequences (5′→3′)
GAPDHF: CTGGGCTACACTGAGCACC
R: AAGTGGTCGTTGAGGGCAATG
PPAR-γF: GGGATCAGCTCCGTGGATCT
R: TGCACTTTGGTACTCTTGAAGTT
SREBP-1cF: GCCCCTGTAACGACCACTG
R: CAGCGAGTCTGCCTTGATG
FASNF: AAGGACCTGTCTAGGTTTGATGC
R: TGGCTTCATAGGTGACTTCCA
PPAR-αF: ATGGTGGACACGGAAAGCC
R: CGATGGATTGCGAAATCTCTTGG
CPT1F: ATCAATCGGACTCTGGAAACGG
R: TCAGGGAGTAGCGCATGGT
ACOX1F: AATCGGGACCCATAAGCCTTT
R: GGGAATACGATGGTTGTCCATTT
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副干酪乳酪杆菌CCFM1224后生元通过调节脂质代谢缓解皮脂代谢紊乱
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卢勇莉 1 , 唐鑫 1 , 潘正浩 1 , 刘飞 1 , 毛丙永 1 , 张秋香 1 , 王伯韬 1, 2 , 赵建新 1 , 石海宁 1, 2 , 陈卫 1 , 崔树茂 1
微生物学报 | 研究报告 2026,66(4): 1941-1955
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微生物学报 | 研究报告 2026, 66(4): 1941-1955
副干酪乳酪杆菌CCFM1224后生元通过调节脂质代谢缓解皮脂代谢紊乱
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卢勇莉1, 唐鑫1 , 潘正浩1, 刘飞1, 毛丙永1, 张秋香1, 王伯韬1, 2, 赵建新1, 石海宁1, 2, 陈卫1, 崔树茂1
作者信息
  • 1.江南大学 食品学院，江苏 无锡
  • 2.华熙生物科技股份有限公司，山东 济南
Lacticaseibacillus paracasei CCFM1224 postbiotics alleviate sebum metabolism disorders by regulating lipid metabolism
Yongli LU1, Xin TANG1 , Zhenghao PAN1, Fei LIU1, Bingyong MAO1, Qiuxiang ZHANG1, Botao WANG1, 2, Jianxin ZHAO1, Haining SHI1, 2, Wei CHEN1, Shumao CUI1
Affiliations
  • 1.School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu, China
  • 2.Bloomage Biotechnology Co. , Ltd. , Jinan, Shandong, China
出版时间: 2026-04-04 doi: 10.13343/j.cnki.wsxb.20260111
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摘要
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目的 皮脂代谢紊乱是多种皮肤疾病的重要诱因，后生元作为一种新兴的微生态制剂显示出调控代谢的潜力。本研究旨在探究副干酪乳酪杆菌CCFM1224后生元对皮脂代谢紊乱的改善作用及其机制，并进一步探索后生元起效组分。 方法 通过构建油酸诱导的小鼠皮脂代谢紊乱模型，从表观指标、激素指标、皮肤脂质含量水平综合评价CCFM1224后生元对皮脂紊乱的改善效果，并检测皮肤脂质代谢相关基因表达变化。利用游离脂肪酸诱导的HepG2细胞脂质堆积模型对后生元功效组分进行筛选。 结果 CCFM1224后生元能显著缓解小鼠皮脂代谢紊乱导致的体重异常增长与睾丸系数增大，减轻皮肤组织病理损伤，降低炎症因子IL-6、IL-1β和TNF-α水平，并下调皮肤组织中甘油三酯(triglyceride, TG)及游离脂肪酸(non-esterified fatty acid, NEFA)含量。机制研究表明，CCFM1224后生元通过抑制脂质合成基因(FASN、PPAR-γ、SREBP-1c)的表达，促进脂质分解基因(PPAR-α、HSL、ATGL)的表达，从而调节皮脂代谢。细胞实验表明，CCFM1224后生元灭活菌体成分能够显著减轻细胞脂质积累及相关损伤，说明其为CCFM1224后生元发挥功效的主要活性组分。 结论 副干酪乳酪杆菌CCFM1224能够通过调节激素分泌以及脂质代谢途径缓解皮脂代谢紊乱，其关键功效物质为灭活菌体组分而非发酵上清液。本研究为后生元在脂质代谢紊乱调控中的应用提供了理论依据，也为相关功能性微生物制剂的开发奠定了研究基础。

副干酪乳酪杆菌  /  后生元  /  皮脂代谢紊乱  /  脂质代谢  /  灭活菌体

Objective Sebum metabolism disorders are a key contributing factor to various dermatological conditions. As an emerging class of microbial agents, postbiotics show potential in regulating metabolic processes. This study aimed to investigate the efficacy and mechanisms of Lacticaseibacillus paracasei CCFM1224 postbiotics in alleviating sebum metabolism disorders and explore the active components responsible for the effects. Methods Using a mouse model of oleic acid-induced sebum metabolism disorders, we comprehensively evaluated the efficacy of CCFM1224 postbiotics in ameliorating sebum imbalance. This evaluation encompassed phenotypic measurements, hormonal parameters, and skin lipid content. Changes in the expression of genes related to skin lipid metabolism were measured via real-time quantitative PCR. Subsequently, a free fatty acid-induced lipid accumulation model in HepG2 cells was utilized to screen the active components of postbiotics. Results CCFM1224 postbiotics significantly ameliorated sebum metabolism disorders in mice. This was evidenced by mitigated abnormal weight gain, a reduced testicle index, alleviated histopathological skin damage, and decreased levels of inflammatory cytokines (IL-6, IL-1β, and TNF-α) as well as triglyceride (TG) and non-esterified fatty acid (NEFA) in the skin tissue. CCFM1224 postbiotics modulated sebum metabolism by downregulating the expression of lipogenesis-related genes (FASN, PPAR-γ, and SREBP-1c) and upregulating the expression of lipolysis-related genes (PPAR-α, HSL, and ATGL). Further cellular validation identified the inactivated bacterial cell component as the key functional fraction, which effectively alleviated intracellular lipid accumulation and associated damage, thereby clarifying the material basis for the effects of CCFM1224 postbiotics. Conclusion L. paracasei CCFM1224 ameliorate sebum metabolism disorders by modulating hormone secretion and lipid metabolic pathways. The key bioactive components were identified as the inactivated bacterial cells, rather than the fermentation supernatant. This finding provides a theoretical foundation for the application of postbiotics in regulating lipid metabolism disorders and establishes a basis for developing related functional microbial preparations.

Lacticaseibacillus paracasei  /  postbiotic  /  sebum metabolism disorders  /  lipid metabolism  /  inactivated bacterial cells
卢勇莉, 唐鑫, 潘正浩, 刘飞, 毛丙永, 张秋香, 王伯韬, 赵建新, 石海宁, 陈卫, 崔树茂. 副干酪乳酪杆菌CCFM1224后生元通过调节脂质代谢缓解皮脂代谢紊乱. 微生物学报, 2026 , 66 (4) : 1941 -1955 . DOI: 10.13343/j.cnki.wsxb.20260111
Yongli LU, Xin TANG, Zhenghao PAN, Fei LIU, Bingyong MAO, Qiuxiang ZHANG, Botao WANG, Jianxin ZHAO, Haining SHI, Wei CHEN, Shumao CUI. Lacticaseibacillus paracasei CCFM1224 postbiotics alleviate sebum metabolism disorders by regulating lipid metabolism[J]. Acta Microbiologica Sinica, 2026 , 66 (4) : 1941 -1955 . DOI: 10.13343/j.cnki.wsxb.20260111
正文
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皮脂是皮肤屏障的重要组成部分，其代谢平衡对维持皮肤生理功能至关重要[1]。皮脂分泌失调会诱导角质形成细胞增殖，加剧角蛋白异常合成和不完全角化，促使炎症性细胞因子过度表达，引起皮肤中的炎症和脂质代谢紊乱[2]，从而破坏皮肤屏障功能，导致痤疮、脂溢性皮炎、银屑病等皮肤疾病的发生[3-4]。皮脂代谢紊乱可能由激素变化(如雄激素)、炎症、微生物群失衡以及环境暴露(如紫外线和污染)等引起[5]。目前常用治疗方案如抗生素和异维A酸等虽具有一定疗效，但存在诸多局限性，包括耐药性、肝毒性、致畸性及其他不良反应，因此亟需探索更为安全、精准的干预策略[6]。
近年来，益生菌被证实可通过减轻炎症与氧化应激、调节皮脂生成和皮肤胰岛素信号传导、抑制致病菌感染等多种途径改善皮脂代谢紊乱[7-8]。值得注意的是，有研究发现灭活益生菌(如乳酸杆菌)在缓解皮肤炎症方面表现出与活菌相似的效应[9-10]。后生元被定义为对宿主健康有益的无生命微生物和/或其成分的制剂，包括无生命的菌体、菌代谢产物和/或菌裂解后成分[11]。与益生菌相比，后生元具有稳定性高、安全性好、易于储存和运输的显著优势，且避免了菌株活性和定植能力的限制[12]，展现出良好的应用前景。尽管已有研究证实后生元在调节代谢和抗炎方面的潜力[13]，但关于后生元调节皮脂代谢紊乱的具体效果及物质基础的研究仍十分有限。前期研究已证实，副干酪乳酪杆菌CCFM1224后生元能够通过调节脂质代谢有效缓解高脂饮食诱导的小鼠非酒精性脂肪肝病[14]。皮脂代谢与机体整体脂质代谢网络密切关联，肝脏作为机体脂质合成、分解与转运的核心器官，其脂质代谢稳态失衡可通过血液循环影响皮肤的脂质合成与分泌过程，而皮肤脂质代谢紊乱也会反向调控肝脏脂质代谢相关通路的表达[15-16]。因此，CCFM1224后生元能否通过调节脂质代谢来改善皮脂代谢紊乱，其具体的功效物质基础及分子机制尚不明确。
本研究通过构建油酸诱导的小鼠皮脂代谢紊乱模型，系统评估副干酪乳酪杆菌CCFM1224后生元对皮脂代谢紊乱的改善作用，并深入分析皮肤组织中脂质代谢关键基因的表达变化，明确其调控皮脂代谢的分子机制。为探索CCFM1224后生元的功效物质基础，本研究进一步利用游离脂肪酸(free fatty acid, FFA)诱导的HepG2细胞脂质代谢紊乱模型，评估CCFM1224后生元发酵上清和灭活菌体成分对细胞脂质代谢紊乱的改善效果。
1 材料与方法
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1.1 菌株和细胞
副干酪乳酪杆菌CCFM1224由江南大学食品微生物菌种保藏中心(Culture Collection of Food Microorganisms, CCFM)提供。人肝癌细胞株HepG2，购自中国科学院上海细胞研究所。
1.2 主要试剂和仪器
酪蛋白胨，上海麦克林生化科技股份有限公司；酵母粉，安琪酵母股份有限公司；MgSO4·7H2O、MnSO4·H2O、K2HPO4·3H2O、液体石蜡，国药集团化学试剂有限公司；中性多聚甲醛固定液、BCA蛋白浓度测定试剂盒、RIPA裂解液，上海碧云天生物技术股份有限公司；UNIQ-10柱TRIzol总RNA分离试剂盒，生工生物工程(上海)股份有限公司；小鼠白细胞介素-6 (interleukin-6, IL-6)、白细胞介素-1β(interleukin-1β, IL-1β)、肿瘤坏死因子-α (tumor necrosis factor-α, TNF-α) ELISA试剂盒，R&D Systems公司；CCK8试剂盒、HiScript® III RT SuperMix for qPCR (+gDNA wiper)、ChamQ Universal SYBR qPCR Master Mix，南京诺唯赞生物科技股份有限公司；RPMI-1640培养基、胎牛血清、青链霉素合剂，Gibco公司；甘油三酯(triglyceride, TG)测试盒、总胆固醇(total cholesterol, TC)测试盒、谷丙转氨酶(alanine aminotransferase, ALT)测试盒、谷草转氨酶(aspartate aminotransferase, AST)测试盒、游离脂肪酸(non-esterified fatty acid, NEFA)测试盒、睾酮测试盒、胰岛素测试盒，南京建成生物工程研究所；油酸、棕榈酸，Sigma-Aldrich公司。
HWS-150恒温培养箱，上海森信实验仪器有限公司；实时定量PCR仪器、实时定量基因扩增仪，Bio-Rad公司；高速冷冻离心机，Eppendorf公司；MLS-3750蒸汽灭菌锅，SANYO公司；高通量组织研磨机、冷冻干燥机，宁波新芝生物科技股份有限公司；切片电子扫描仪，匈牙利3DHISTECH公司；Multiscan Go多功能酶标仪，上海智诚有限公司。
1.3 后生元制备
将副干酪乳酪杆菌CCFM1224菌株在MRS培养基[14]中培养，初始菌浓度为5×107-1×108 CFU/mL，37 ℃培养30 h。发酵液经热处理(65 ℃，30 min)和超声处理(功率60%，15 min)后冻干，即获得动物实验所需后生元；发酵液4 ℃、8 000×g离心15 min，将上清液进行过滤除菌，菌体进行灭活处理后冻干备用，即获得细胞实验所需后生元组分。通过平板计数法验证灭活效果，冻干后菌体稀释涂布MRS平板37 ℃培养48 h后进行菌落计数，菌落数<103 CFU/mL，确定为细菌菌体几乎完全失活[17]，冻干后的样品在-80 ℃储存。
1.4 动物实验设计
本研究所有动物实验得到江南大学实验动物伦理委员会的批准，编号为JN. No20220530c0950720[174]。20只6周龄的雄性C57BL/6N小鼠购自北京维通利华实验动物技术有限公司，适应1周(自由摄食标准饲料和饮水)后进行随机分组，每组5只，实验期间所有小鼠均饲喂标准饲料。采用油酸诱导建立小鼠皮脂代谢紊乱模型[18]，该模型通过局部皮肤涂抹油酸，能够有效模拟皮脂代谢紊乱状态下皮脂腺过度增殖、脂质分泌异常及局部炎症反应等核心病理特征，且造模方法简便、造模成功率高，模型稳定性好，能够有效反映受试物对皮脂代谢紊乱的改善作用[19-20]。具体造模及干预过程如下：对所有小鼠背部约4 cm2区域进行脱毛处理，实验组和模型组小鼠每日在背部脱毛处皮肤涂抹60 µL 65%油酸，连续处理21 d；空白组则用等体积100%液体石蜡进行相同处理。从造模首日起同步进行灌胃干预，连续干预21 d，小鼠具体分组及干预情况见表1。实验结束后，小鼠麻醉后摘眼球取血并辅以脱颈处死，收集皮肤组织(脱毛处理部分)和睾丸。全血静置2 h后以3 000 r/min离心10 min后获得血清，置于-80 ℃保存。睾丸系数计算如公式(1)所示。
Ct=Wt/Wb×100
式中：Ct为睾丸系数(%)，Wt为双侧睾丸重量(g)，Wb为小鼠体重(g)。
1.5 皮肤组织病理学分析
将小鼠皮肤组织在4%多聚甲醛中固定48 h后，进行脱水、石蜡包埋和切片制作，并用苏木精和伊红(hematoxylin-eosin, H&E)染色[21]，使用数字切片扫描仪对切片进行扫描分析。
1.6 炎症因子含量测定
根据说明书检测小鼠皮肤组织中的炎症细胞因子(TNF-α、IL-6和IL-1β)的含量。
1.7 皮肤脂质和血清激素水平的测定
根据说明书检测皮肤组织中TG和游离脂肪酸(non-esterified fatty acid, NEFA)含量以及小鼠血清中的睾酮和胰岛素含量。
1.8 实时荧光定量逆转录PCR (real-time RT-PCR, RT-qPCR)
使用总RNA分离试剂盒从小鼠皮肤组织或HepG2细胞中提取总RNA，之后使用逆转录试剂盒将RNA逆转录为cDNA，采用ChamQ Universal SYBR qPCR Master Mix预混样本，使用384孔板荧光定量PCR仪进行RT-qPCR反应，以GAPDH为内参基因，检测脂质代谢相关基因的表达。PCR反应体系(10 µL)：Taq Pro Universal SYBR qPCR Master Mix 5 µL，正、反向引物(10 µmol/L)各0.25 µL，模板DNA (10 ng/µL) 1 µL，双蒸水3.5 µL。反应程序：95 ℃ 30 s；95 ℃ 10 s，60 ℃ 10 s，循环30次。建立熔化曲线时，从65 ℃开始，每5 s增加0.5 ℃，增加到95 ℃。最后采用2-△△Ct法处理数据，计算基因的相对表达量。动物实验所用引物序列见表2，细胞实验所用引物序列见表3。
1.9 细胞培养
HepG2细胞置于添加10%胎牛血清和1%青霉素/链霉素的RPMI-1640培养基，在恒温培养箱(37 ℃、5% CO2)中培养。待细胞80%贴壁后，进行分组干预处理。
1.10 细胞毒性实验
将细胞以1×104个/孔的密度接种于96孔板培养24 h后，吸出培养上清液，用无菌PBS溶液洗涤2-3次，使用含有不同浓度梯度干预物质的培养基继续培养24 h，每组3个平行。根据CCK8试剂盒说明书要求，用CCK8法检测细胞活力。
1.11 细胞造模及干预
HepG2细胞脂质代谢紊乱模型采用1 mmol/L游离脂肪酸(free fatty acids, FFA) (油酸:棕榈酸=2:1)诱导建立[22]。细胞分组为空白对照组(Control，培养基培养)、模型组(Model，含FFA的培养基培养)、CCFM1224发酵上清组(CCFM1224-FS、含FFA和CCFM1224发酵上清的培养基培养)、CCFM1224灭活菌体组(CCFM1224-IB、含FFA和CCFM1224灭活菌体的培养基培养)。
1.12 细胞生化指标测定
将细胞以2×105个/孔的密度接种于6孔板上，当细胞密度接近70%时，按1.11节的分组进行干预处理，继续培养24 h后，收集各孔细胞上清液，测定各孔细胞培养上清液中ALT、AST含量；细胞使用RIPA裂解液裂解后，测定胞内TG和TC的含量。
1.13 统计学方法
使用GraphPad Prism 10.1.2进行统计分析和绘图，使用Tukey检验进行的方差分析用于确定组间差异性。实验数据以平均值±标准差(SD)表示，统计显著性表示如下：*：P<0.05；**：P<0.01；***：P<0.001。
2 结果与分析
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2.1 CCFM1224后生元对小鼠体重和睾丸系数的影响
各组小鼠体重增加量及睾丸系数如图1所示，与空白对照组相比，模型组小鼠体重增加量显著降低55.98% (P<0.001)，睾丸系数则升高了32.25% (P<0.001)，表明油酸诱导显著抑制小鼠体重的正常增长，并引起睾丸系数异常增大。在CCFM1224后生元口服干预后，小鼠的体重增加量较模型组回升83.35% (P<0.001)，睾丸系数下降18.14% (P<0.01)，而培养基干预组则未见显著改善。结果表明，CCFM1224后生元干预能够有效缓解油酸诱导所致的小鼠体重不正常增长以及睾丸系数增大的现象。
2.2 CCFM1224后生元对小鼠皮肤组织病理学及炎症因子的影响
为进一步明确油酸诱导造模对小鼠皮肤组织形态的影响及CCFM1224后生元的干预效果，采用H&E染色法对小鼠皮肤组织进行观察，结果如图2所示。油酸诱导造模后，模型组小鼠与空白对照组相比皮肤结构组织差异变化显著，具体表现为表皮鳞状上皮层显著增厚并伴有角化过度，真皮层有明显血管充血，炎症细胞浸润显著，皮脂腺增生肿大且形状不规则。经CCFM1224后生元干预后，小鼠皮肤组织的病理异常得到明显缓解，皮脂腺体积缩小，皮肤角化过度现象显著改善，真皮层炎症细胞浸润数量大幅减少。培养基干预组小鼠的皮肤组织形态与模型组相比无显著差异。
如图2所示，与空白对照组相比，模型组小鼠皮肤组织中相关的炎症细胞因子IL-6、IL-1β和TNF-α的含量显著升高(P<0.001)。CCFM1224后生元干预后，小鼠皮肤炎症状态得到有效缓解。与模型组相比，CCFM1224后生元干预组小鼠皮肤组织中IL-6、IL-1β和TNF-α的含量分别显著降低了27.44% (P<0.01)、29.35% (P<0.001)和36.11% (P<0.001)，培养基处理则对皮肤的炎症因子水平无显著的影响。上述结果表明，CCFM1224后生元不仅能够显著改善油酸诱导造模引起的小鼠皮肤组织病理病变，还可有效减轻小鼠皮肤的炎症反应。
2.3 CCFM1224后生元对小鼠皮肤脂质含量的影响
皮脂是由多种脂质组成的混合物，其中TG和NEFA是皮肤组织中含量最丰富的脂类成分，其中TG水平过高可导致皮脂腺增生肥大，NEFA水平异常升高则会诱发导管角化异常，进而损伤皮肤屏障功能[23]。为更直观地明确皮肤组织中脂质组分的变化特征，本研究对皮肤组织中TG及NEFA的含量进行了检测。如图3所示，油酸诱导后，小鼠皮肤组织中TG和NEFA含量均显著升高，与空白对照组相比，模型组2种脂质含量分别增加106.75% (P<0.001)和98.49% (P<0.001)；而相比模型组，口服CCFM1224后生元干预后，小鼠皮肤组织中TG和NEFA含量分别下降39.06% (P<0.01)和46.04% (P<0.001)，而培养基干预组与模型组相比，2种脂质含量无显著差异。结果表明，CCFM1224后生元能够有效降低油酸诱导引起的TG和NEFA含量异常升高，改善皮肤脂质代谢紊乱状态。
2.4 CCFM1224后生元对小鼠血清激素分泌的影响
为探究CCFM1224后生元对激素水平的影响，本研究检测了小鼠血清中睾酮与胰岛素的含量。如图4所示，与空白对照组相比，模型组小鼠血清睾酮和胰岛素水平分别显著升高51.27% (P<0.01)和112.05% (P<0.001)，经CCFM1224后生元干预后，上述指标较模型组分别降低了27.78% (P<0.01)和33.48% (P<0.01)，培养基组未见显著变化。结果表明，CCFM1224后生元能够有效抑制油酸诱导的血清睾酮和胰岛素水平异常上升，从而缓解皮脂代谢紊乱。
2.5 CCFM1224后生元调节皮脂代谢的机制
上述研究证实CCFM1224后生元能够调节皮脂代谢紊乱，为进一步研究其调节皮脂代谢的机制，对皮肤组织中脂质代谢相关基因的表达水平进行了分析。如图5所示，油酸诱导后模型组中的脂质合成相关基因，包括脂肪酸合成酶(fatty acid synthetase)基因FASN、过氧化物酶体增殖物激活受体γ (peroxisome-proliferator-activated receptor γ)基因PPAR-γ和固醇调节元件结合蛋白-1c (sterol regulatory element-binding protein 1c)基因SREBP-1c的表达水平较空白对照组分别显著上调112.41% (P<0.001)、77.22% (P<0.001)和72.56% (P<0.001)，而脂质分解相关基因的表达则呈现不同趋势：过氧化物酶体增殖物激活受体α (peroxisome-proliferator-activated receptor α)基因PPAR-α的表达水平较空白对照组下调36.57% (P<0.001)、脂肪甘油三酯脂肪酶(adipose triglyceride lipase)基因ATGL的表达水平较空白对照组略有上调(P<0.05)、激素敏感性脂肪酶(hormone-sensitive lipase)基因HSL的表达水平较空白对照组则无显著变化，说明油酸干预促进了皮肤脂质合成并在一定程度上抑制其分解。经CCFM1224后生元干预后，与模型组相比，FASN、PPAR-γ和SREBP-1c的表达水平分别降低了41.29% (P<0.001)、36.07% (P<0.001)和28.19% (P<0.001)，PPAR-α、HSL和ATGL的表达分别升高63.55% (P<0.001)、43.83% (P<0.001)和59.09% (P<0.001)。上述结果表明，CCFM1224后生元可通过抑制脂质合成基因表达并促进脂质分解基因表达，双向调节皮肤脂质代谢过程，从而改善皮脂分泌异常。
2.6 CCFM1224后生元功效物质筛选
上述动物实验结果证明CCFM1224后生元能够通过调节脂质代谢从而缓解皮脂代谢紊乱，为进一步探索后生元调节皮脂代谢紊乱的功效组分，将后生元分为发酵上清和灭活菌体成分，通过HepG2细胞脂质代谢紊乱模型，进一步确定后生元功效组分。
为确定CCFM1224后生元发酵上清(fermentation supernatant, FS)与灭活菌体(inactivated bacteria, IB)的安全干预浓度，首先评估了二者对HepG2细胞活力的影响。如图6所示，在不同浓度处理下，FS与IB组的细胞活力均维持在较高水平，与空白对照组相比，FS在0-40 μg/mL浓度范围内、IB在0-80 μg/mL浓度范围内均未对细胞活力产生显著抑制，表明在此浓度区间内2种组分均无明显细胞毒性。当FS浓度达到80 μg/mL、IB浓度达到160 μg/mL时，细胞活力显著下降。基于上述结果，本研究选取对细胞活性无显著影响的最高浓度作为后续实验干预剂量，即CCFM1224的FS和IB的干预浓度分别为40 μg/mL和80 μg/mL。
细胞脂质代谢紊乱可导致胞内脂质异常蓄积并引发细胞损伤[24]，为评估后生元不同组分对脂质堆积及细胞完整性的影响，本研究检测了细胞内TG与TC水平，以及细胞培养上清液中ALT和AST的含量。如图7所示，经FFA诱导后，细胞内TG、TC含量及上清液中ALT、AST水平均显著升高。CCFM1224-IB干预后，细胞内TG和TC含量分别降低40.2% (P<0.001)和23.45% (P<0.001)，同时上清中ALT和AST释放量也分别下降27.66% (P<0.001)和22.52% (P<0.001)。相比之下，CCFM1224-FS处理对FFA诱导的胞内脂质蓄积及细胞损伤均未表现出显著改善作用。结果表明，CCFM1224-IB能够同时减轻细胞脂质堆积并保护细胞结构完整性，而CCFM1224-FS则无明显效果。
为进一步探究CCFM1224后生元不同组分对脂质代谢的调控机制，本研究分析了HepG2细胞中脂质代谢相关基因的表达情况。如图8所示，FFA诱导后，模型组脂质合成相关基因PPAR-γ、SREBP-1c及FASN的表达均显著上调(P<0.001)，而脂质氧化分解相关基因PPAR-α、肉碱棕榈酰基转移酶1 (carnitine palmitoyltransferase)基因CPT1和酰基辅酶A氧化酶1 (acyl-CoA oxidase 1)基因ACOX1的表达则显著下调(P<0.001)，表明FFA干预促进了细胞脂质合成并抑制了其分解代谢。经CCFM1224-IB干预后，与模型组相比，PPAR-γ、SREBP-1c和FASN的表达分别下调29.68% (P<0.01)、26.89% (P<0.01)和28.46% (P<0.01)，同时，PPAR-α、CPT1和ACOX1的表达分别上调77.79% (P<0.001)、95.42% (P<0.001)和43.36% (P<0.01)。CCFM1224-FS干预组中PPAR-α和CPT1的表达也有所上调(P<0.05)，但幅度低于IB组，且对PPAR-γ、SREBP-1c、FASN及ACOX1的表达均无显著影响。综上所述，CCFM1224的灭活菌体组分能够通过抑制脂质合成以及促进脂质氧化分解有效调节FFA诱导的细胞脂质代谢紊乱，而发酵上清组分在基因层面的调节作用相对有限。
3 讨论与结论
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皮脂代谢紊乱是痤疮、脂溢性皮炎等皮肤疾病的关键诱因，其发生发展与激素水平、局部炎症及脂质合成与分解失衡密切相关[25-26]。现有治疗药物常伴有一定副作用，因此探索安全有效的微生态调控策略具有重要意义。益生菌后生元为益生菌代谢产物或灭活菌体，具有安全、稳定且易吸收的优势，已被证实在调节代谢、抗炎等方面发挥重要作用[27]。本研究通过动物实验与细胞实验相结合，系统探究了副干酪乳酪杆菌CCFM1224后生元对油酸诱导的小鼠皮脂代谢紊乱的干预效果、作用机制及功效组分。
动物实验结果显示，油酸诱导可显著抑制小鼠体重正常增长、使睾丸系数异常增大，同时导致皮肤组织病理损伤、炎症因子异常升高及脂质代谢紊乱，这与已有研究中油酸诱导代谢紊乱模型的特征一致[28]。CCFM1224后生元干预可有效逆转上述异常，显著回升小鼠体重增加量、降低睾丸系数，改善皮肤表皮增厚、角化过度及炎症浸润等病理表现，同时下调皮肤组织IL-6、IL-1β和TNF-α等炎症因子含量，降低皮肤组织TG、NEFA水平。
激素水平异常是皮脂代谢紊乱的重要调控因素，睾酮与胰岛素均可通过促进皮脂腺增生、加速脂质合成，诱发皮脂分泌过多[29]。本研究发现，CCFM1224后生元可显著降低油酸诱导的小鼠血清睾酮和胰岛素水平异常升高，这提示其可能通过调节内分泌系统稳态，间接改善皮脂代谢紊乱。
皮脂代谢的稳态调控依赖于脂质合成与分解过程的动态平衡，这一过程受多种关键基因的协同调控，其表达异常是导致皮脂代谢紊乱重要分子机制[30]。进一步机制探究表明，CCFM1224后生元可双向调控皮肤组织脂质代谢相关基因表达，显著抑制FASN、PPAR-γ和SREBP-1c等脂质合成基因的表达，同时促进PPAR-α、HSL和ATGL等脂质分解基因的表达，FASN是脂肪酸从头合成的关键限速酶，PPAR-γ和SREBP-1c为脂质合成的核心转录调控因子；PPAR-α、激素HSL及ATGL是脂质氧化分解通路的关键基因[30-31]。从基因表达层面清晰地揭示了其恢复皮脂代谢动态平衡的机制，明确了CCFM1224后生元调节皮肤脂质代谢的分子路径(图9)。
为筛选CCFM1224后生元中发挥功效的主要组分，本研究将其分为FS与IB组分，通过HepG2细胞脂质代谢紊乱模型验证发现，IB组分是其发挥功效的关键。研究表明，IB组分可显著降低FFA诱导的细胞内TG、TC含量，减少ALT、AST释放，保护细胞结构完整性，同时通过抑制脂质合成基因、促进脂质氧化分解基因表达，有效调节细胞脂质代谢紊乱；而FS组分仅轻微上调部分脂质分解基因表达，无显著整体干预效果。这表明，菌体结构成分或其附着的特定成分可能在调控脂代谢中扮演关键角色。已有文献报道，来自副干酪乳杆菌的脂磷壁酸能够通过调控TLR4-MyD88-MAPK和NF-κB信号通路来减轻炎症反应[32]；乳杆菌来源的表面层蛋白可调节肠道菌群并抑制肝脏脂质合成基因的表达[33]。基于此，推测本研究副干酪乳酪杆菌CCMF1224后生元的关键功效物质可能来源于其灭活菌体组分中的特定成分。然而，关于该活性物质的具体化学本质及其与宿主细胞相互作用的精细分子机制，仍有待进一步地分离纯化与深入的功能验证。
本研究仍存在一定局限性：(1) 本研究采用的油酸局部涂抹诱导的小鼠皮脂代谢紊乱模型，模拟皮脂代谢紊乱时皮脂腺过度增殖、局部炎症及皮肤屏障功能损伤等综合病理状态，该模型仅模拟了脂质代谢紊乱的单一诱因，与人体皮脂代谢紊乱的病理状态存在差异，后续需建立更贴近临床的动物模型验证其功效；(2) 采用HepG2肝细胞模型筛选功效组分并探究脂质代谢调控机制，虽脂质代谢核心通路在不同细胞中具有共通性，但HepG2细胞与皮肤皮脂腺细胞存在明显的细胞类型差异，后续研究将选用皮脂腺细胞(如人HaCaT细胞或原代皮脂腺细胞)进一步验证CCFM1224灭活菌体对皮脂代谢的直接调控作用及机制；(3) CCFM1224灭活菌体的具体功效成分尚未明确，需通过进一步地分离纯化挖掘其活性物质结构。
综上所述，本研究证实CCFM1224后生元可通过调节激素分泌、减轻炎症反应、调控脂质代谢相关基因表达，有效缓解油酸诱导的皮脂代谢紊乱，且初步确定其灭活菌体为主要功效组分。本研究丰富了后生元调节皮脂代谢的研究内容，为后生元在皮脂代谢紊乱调控中的应用提供了理论依据，也为相关功能性微生物制剂的开发奠定了研究基础。
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2026年第66卷第4期
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doi: 10.13343/j.cnki.wsxb.20260111
  • 接收时间：2026-02-05
  • 首发时间：2026-04-14
  • 出版时间：2026-04-04
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  • 收稿日期：2026-02-05
  • 录用日期：2026-03-03
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    1.江南大学 食品学院，江苏 无锡
    2.华熙生物科技股份有限公司，山东 济南
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2种不同金属材料的力学参数
科
Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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