留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

不良饮食习惯影响瘢痕疙瘩形成的研究进展

徐琦 刘伟

徐琦, 刘伟. 不良饮食习惯影响瘢痕疙瘩形成的研究进展[J]. 中华烧伤与创面修复杂志, 2022, 38(4): 389-393. DOI: 10.3760/cma.j.cn501120-20210401-00112.
引用本文: 徐琦, 刘伟. 不良饮食习惯影响瘢痕疙瘩形成的研究进展[J]. 中华烧伤与创面修复杂志, 2022, 38(4): 389-393. DOI: 10.3760/cma.j.cn501120-20210401-00112.
Xu Q,Liu W.Research advances on the influence of poor dietary habits on the development of keloids[J].Chin J Burns Wounds,2022,38(4):389-393.DOI: 10.3760/cma.j.cn501120-20210401-00112.
Citation: Xu Q,Liu W.Research advances on the influence of poor dietary habits on the development of keloids[J].Chin J Burns Wounds,2022,38(4):389-393.DOI: 10.3760/cma.j.cn501120-20210401-00112.

不良饮食习惯影响瘢痕疙瘩形成的研究进展

doi: 10.3760/cma.j.cn501120-20210401-00112
基金项目: 

国家自然科学基金面上项目 81671921

详细信息
    通讯作者:

    刘伟,Email:liuwei_md@126.com

Research advances on the influence of poor dietary habits on the development of keloids

Funds: 

General Program of National Natural Science Foundation of China 81671921

More Information
    Corresponding author: Liu Wei, Email: liuwei_md@126.com
  • 摘要: 长期的不良饮食习惯可造成肠道菌群改变,使得内毒素/脂多糖大量生成,导致肠道黏膜通透性增加,激活大量炎症因子进入门静脉。此外,高碳水化合物饮食可增加肝脏代谢负担,促进线粒体氧化磷酸化,导致氧化应激,在ATP合成过程中产生新的脂肪,从而导致脂肪异位堆积,激活核因子κB信号通路,释放肿瘤坏死因子α、白细胞介素1β(IL-1β)和IL-6等炎症因子,导致肥胖和胰岛素抵抗,最终引发系统性低度炎症。该综述回顾了不良饮食习惯导致系统性低度炎症的机制、瘢痕疙瘩与系统性低度炎症的临床研究与实验研究进展、饮食习惯与瘢痕疙瘩体质的关联性,提出了不良饮食习惯可能导致瘢痕疙瘩发生与发展的假说。

     

  • 参考文献(38)

    [1] KendallAC,NicolaouA.Bioactive lipid mediators in skin inflammation and immunity[J].Prog Lipid Res,2013,52(1):141-164.DOI: 10.1016/j.plipres.2012.10.003.
    [2] 刘伟.瘢痕疙瘩发生和发展的整体观机制探讨[J].组织工程与重建外科杂志,2018,14(4):181-183. DOI: 10.3969/j.issn.1673-0364.2018.04.001.
    [3] CalderPC, AhluwaliaN, BrounsF, et al. Dietary factors and low-grade inflammation in relation to overweight and obesity[J]. Br J Nutr,2011,106 (Suppl 3):S5-78. DOI: 10.1017/S0007114511005460.
    [4] CalderPC,AhluwaliaN,AlbersR,et al. A consideration of biomarkers to be used for evaluation of inflammation in human nutritional studies[J].Br J Nutr,2013,109 (Suppl 1):S1-34.DOI: 10.1017/S0007114512005119.
    [5] O'HaraAM, ShanahanF. The gut flora as a forgotten organ[J]. EMBO Rep,2006,7(7): 688-693. DOI: 10.1038/sj.embor.7400731.
    [6] GuoZ, LiuXM, ZhangQX, et al. Influence of consumption of probiotics on the plasma lipid profile: a meta-analysis of randomised controlled trials[J]. Nutr Metab Cardiovasc Dis, 2011,21(11): 844-850. DOI: 10.1016/j.numecd.2011.04.008.
    [7] de VreseM,SchrezenmeirJ.Probiotics, prebiotics, and synbiotics[J].Adv Biochem Eng Biotechnol,2008,111:1-66.DOI: 10.1007/10_2008_097.
    [8] NagataE, OhoT. Invasive Streptococcus mutans induces inflammatory cytokine production in human aortic endothelial cells via regulation of intracellular toll-like receptor 2 and nucleotide-binding oligomerization domain 2[J]. Mol Oral Microbiol,2017,32(2):131-141. DOI: 10.1111/omi.12159.
    [9] CaniPD, AmarJ, IglesiasMA, et al. Metabolic endotoxemia initiates obesity and insulin resistance[J]. Diabetes,2007,56(7):1761-1772. DOI: 10.2337/db06-1491.
    [10] CaniPD, BibiloniR, KnaufC, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice[J]. Diabetes,2008,57(6):1470-1481. DOI: 10.2337/db07-1403.
    [11] CaniPD, DelzenneNM. The role of the gut microbiota in energy metabolism and metabolic disease[J]. Curr Pharm Des,2009,15(13):1546-1558. DOI: 10.2174/138161209788168164.
    [12] CrescenzoR,MazzoliA,Di LucciaB,et al.Dietary fructose causes defective insulin signalling and ceramide accumulation in the liver that can be reversed by gut microbiota modulation[J].Food Nutr Res,2017,61(1):1331657.DOI: 10.1080/16546628.2017.1331657.
    [13] CrescenzoR, BiancoF, FalconeI, et al. Increased hepatic de novo lipogenesis and mitochondrial efficiency in a model of obesity induced by diets rich in fructose[J]. Eur J Nutr,2013,52(2):537-545. DOI: 10.1007/s00394-012-0356-y.
    [14] FengRN, DuSS, ChenY, et al. High carbohydrate intake from starchy foods is positively associated with metabolic disorders: a cohort study from a Chinese population[J]. Sci Rep, 2015,5:16919. DOI: 10.1038/srep16919.
    [15] 杨姗姗,胡秀芬,温宇.脂毒性-炎症反应与胰岛素抵抗的关系研究进展[J].生理科学进展,2011,42(2):112-117.
    [16] 刘洋,马世平,吴斐华.胰岛素抵抗与内皮功能紊乱的共同发病机制[J].海峡药学,2010,22(5):115-118.DOI: 10.3969/j.issn.1006-3765.2010.05.050.
    [17] DefronzoRA. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus[J]. Diabetes,2009,58(4):773-795. DOI: 10.2337/db09-9028.
    [18] MatulewiczN, Karczewska-KupczewskaM. Insulin resistance and chronic inflammation[J/OL]. Postepy Hig Med Dosw (Online),2016,70:1245-1258[2021-04-01]. https://pubmed.ncbi.nlm.nih.gov/28026827/. DOI: 10.5604/17322693.1226662.
    [19] SteinB, BaldwinASJr. Distinct mechanisms for regulation of the interleukin-8 gene involve synergism and cooperativity between C/EBP and NF-kappa B[J]. Mol Cell Biol,1993,13(11):7191-7198. DOI: 10.1128/mcb.13.11.7191-7198.1993.
    [20] BoyceDE, CiampoliniJ, RugeF, et al. Inflammatory-cell subpopulations in keloid scars[J]. Br J Plast Surg,2001,54(6):511-516. DOI: 10.1054/bjps.2001.3638.
    [21] OgawaR. Keloid and hypertrophic scars are the result of chronic inflammation in the reticular dermis[J]. Int J Mol Sci,2017,18(3):606. DOI: 10.3390/ijms18030606.
    [22] 高振,武晓莉,李青峰.瘢痕治疗现状与进展[J].临床外科杂志,2020,28(12):1106-1109.DOI: 10.3969/j.issn.1005-6483.2020.12.003.
    [23] 曹振东, 刘伟. 从全身性炎症角度审视瘢痕疙瘩发病机制和治疗策略[J].中华烧伤杂志, 2020,36(5):334-338. DOI: 10.3760/cma.j.cn501120-20200401-00205.
    [24] HuangCY, OgawaR. Systemic factors that shape cutaneous pathological scarring[J]. FASEB J,2020,34(10):13171-13184. DOI: 10.1096/fj.202001157R.
    [25] ArimaJ, HuangCY, RosnerB, et al. Hypertension: a systemic key to understanding local keloid severity[J]. Wound Repair Regen,2015,23(2):213-221. DOI: 10.1111/wrr.12277.
    [26] GhazizadehM. Essential role of IL-6 signaling pathway in keloid pathogenesis[J]. J Nippon Med Sch,2007,74(1):11-22. DOI: 10.1272/jnms.74.11.
    [27] McCauleyRL,ChopraV,LiYY, et al. Altered cytokine production in black patients with keloids[J].J Clin Immunol,1992,12(4):300-308.DOI: 10.1007/BF00918154.
    [28] 赵庆利,张景龙,董静,等.瘢痕疙瘩中医体质类型与临床特征间关系分析[J].中国美容医学,2009,18(11):1670-1672.DOI: 10.3969/j.issn.1008-6455.2009.11.056.
    [29] 刘海洋,董佳容,武晓莉,等.中医痰湿/湿热舌象与体质在瘢痕疙瘩患者中分布的初步调查研究[J].中国美容整形外科杂志,2018,29(10):611-615,后插10-4.DOI: 10.3969/j.issn.1673-7040.2018.10.010.
    [30] Akpinar KaraY, OzdemirD. Evaluation of food consumption in patients with acne vulgaris and its relationship with acne severity[J]. J Cosmet Dermatol,2020,19(8):2109-2113. DOI: 10.1111/jocd.13255.
    [31] SeoYS, LeeHB, KimY, et al. Dietary carbohydrate constituents related to gut dysbiosis and health[J]. Microorganisms,2020,8(3):427. DOl:10.3390/microorganisms8030427.
    [32] Tomaro-DuchesneauC,SahaS,MalhotraM,et al.Probiotic ferulic acid esterase active lactobacillus fermentum NCIMB 5221 APA microcapsules for oral delivery: preparation and in vitro characterization[J].Pharmaceuticals (Basel),2012,5(2):236-248.DOI: 10.3390/ph5020236.
    [33] MakkiK, DeehanEC, WalterJ, et al. The impact of dietary fiber on gut microbiota in host health and disease[J]. Cell Host Microbe,2018,23(6):705-715. DOI: 10.1016/j.chom.2018.05.012.
    [34] OnishiN, KawamotoS, SuzukiH, et al. Dietary pulverized konjac glucomannan suppresses scratching behavior and skin inflammatory immune responses in NC/Nga mice[J]. Int Arch Allergy Immunol,2007,144(2):95-104. DOI: 10.1159/000103220.
    [35] LouwL. Keloids in rural black South Africans. Part 1: general overview and essential fatty acid hypotheses for keloid formation and prevention[J].Prostaglandins Leukot Essent Fatty Acids,2000,63(5):237-245. DOI: 10.1054/plef.2000.0207.
    [36] LouwL, DannhauserA. Keloids in rural black South Africans. Part 2: dietary fatty acid intake and total phospholipid fatty acid profile in the blood of keloid patients[J].Prostaglandins Leukot Essent Fatty Acids,2000,63(5):247-253.DOI: 10.1054/plef.2000.0208.
    [37] LouwL, van der WesthuizenJP, Duyvene de WitL, et al. Keloids: peripheral and central differences in cell morphology and fatty acid compositions of lipids[J]. Adv Exp Med Biol,1997,407:515-520. DOI: 10.1007/978-1-4899-1813-0_77.
    [38] LouwL. Keloids in rural black South Africans. Part 3: a lipid model for the prevention and treatment of keloid formations[J]. Prostaglandins Leukot Essent Fatty Acids,2000,63(5):255-262. DOI: 10.1054/plef.2000.0209.
  • 1  高碳水化合物与高脂饮食习惯导致系统性低度炎症的机制

    注:IL为白细胞介素,MCP-1为单核细胞趋化蛋白1,TNF-α为肿瘤坏死因子α,JNK为c-Jun氨基端激酶,ATP为腺苷三磷酸,LPS为内毒素/脂多糖,TLR为Toll样受体,NOD2为核苷酸结合寡聚化结构域2

  • 加载中
图(1)
计量
  • 文章访问数:  489
  • HTML全文浏览量:  145
  • PDF下载量:  72
  • 被引次数: 0
出版历程
  • 收稿日期:  2021-04-01

目录

    /

    返回文章
    返回