不良饮食习惯影响瘢痕疙瘩形成的研究进展

徐琦; 刘伟

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

徐琦,
刘伟^,

1.
潍坊医学院整形外科研究所，潍坊　　261042
2.
上海交通大学医学院附属第九人民医院整复外科，上海市组织工程研究重点实验室，上海　　200011

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

计量
- 文章访问数: 505
- HTML全文浏览量: 152
- PDF下载量: 72
- 被引次数: 0
出版历程
- 收稿日期: 2021-04-01

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

Xu Qi,
Liu Wei^,

1.
Institute of Plastic Surgery, Weifang Medical University, Weifang 261042, China
2.
Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China

Funds:

General Program of National Natural Science Foundation of China 81671921

More Information

Corresponding author: Liu Wei, Email: liuwei_md@126.com

摘要

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。
- 瘢痕疙瘩 /
- 饮食习惯 /
- 炎症 /
- 胃肠道微生物组 /
- 系统性低度炎症
Abstract: Long-term poor dietary habits can cause changes in the intestinal flora, resulting in the production of a large number of lipopolysaccharide, increase intestinal mucosal permeability, and activate the entrance of a large number of inflammatory factors into the portal vein. In addition, a high carbohydrate diet can increase liver metabolic burden, increase mitochondrial oxidative phosphorylation, leading to oxidative stress, generate new fat during adenosine triphosphate synthesis, and thus resulting in ectopic fat accumulation, which further activate nuclear factor-κB signaling pathway and release inflam- matory factors such as tumor necrosis factor-α, interleukin-1β (IL-1β), IL-6, and so on. This leads to obesity and insulin resis- tance, ultimately triggering systemic low-grade inflammation. This article reviews the mechanism of poor dietary habits leading to systemic low-grade inflammation, the clinical and experimental research progress of keloids and systemic low-grade inflammation, the association between dietary habits and keloid constitution, and puts forward the hypothesis that poor dietary habits may lead to the occurrence and development of keloids.
- Keloid /
- Food habits /
- Inflammation /
- Gastrointestinal microbiome /
- Systemic low-grade inflammation
所有作者均声明不存在利益冲突

HTML全文

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

下载: 全尺寸图片幻灯片