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中药通过调节肠道微生物群与宿主的共生稳态来改善重症肌无力。

Traditional Chinese medicine improves myasthenia gravis by regulating the symbiotic homeostasis of the intestinal microbiota and host.

作者信息

Zhao Mingli, Liu Li, Liu Fanzhao, Liu Lei, Liu Zhijuan, Gao Yanli, Cao Jianxi

机构信息

Department of Cardio-Thoracic Surgery, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China.

Department of Thoracic Surgery, Henan Province Hospital of Traditional Chinese Medicine, Zhengzhou, China.

出版信息

Front Microbiol. 2023 Jan 6;13:1082565. doi: 10.3389/fmicb.2022.1082565. eCollection 2022.

DOI:10.3389/fmicb.2022.1082565
PMID:36687653
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9852828/
Abstract

Myasthenia gravis (MG) is an autoimmune disease caused by autoantibodies that is dependent on T-cell immunity and complement participation and mainly involves neuromuscular junctions. In this study, 30 patients with myasthenia gravis were selected and divided into pretreatment (Case group) and posttreatment (Treatment group) and 30 healthy volunteers (CON group) were included. Among them, the treatment group was treated with Modified Buzhong Yiqi Decoction (MBZYQD), and the levels of antibodies such as AChR, Musk and Titin in blood and intestinal microbiota were compared before treatment (Case group), after treatment (Treatment group) and in healthy volunteers (CON group). The results showed that after treatment with MBZYQD, the antibody levels of AChR, MuSK, and Titin and the inflammatory factor level of IL-6, IL-1β, and IL-22 in MG patients decreased significantly and nearly returned to a healthy level. In addition, after treatment with MBZYQD, the diversity, structure and function of intestinal microorganisms in MG patients also recovered to a healthy level. At the phylum level, the relative abundance of Proteobacteria in the Case group increased significantly, accompanied by a significant decrease in the relative abundance of Bacteroides compared with that in the CON group, the relative abundance of Proteobacteria and Bacteroides in the Treatment group was similar to that in the CON group. At the genus level, the relative abundance of in the Case group was significantly increased, accompanied by a significant decrease in the relative abundance of , and the relative abundance of and in Treatment group was similar to that in the CON group. Moreover, the fluorobenzoate degradation pathway (KO00364) was significantly increased in the Case group, while this pathway was significantly decreased in the Treatment group. In conclusion, MBZYQD can improve the immune function of the host by regulating the diversity, structure and function of the intestinal microbiota to treat myasthenia gravis.

摘要

重症肌无力(MG)是一种由自身抗体引起的自身免疫性疾病,依赖于T细胞免疫和补体参与,主要累及神经肌肉接头。本研究选取30例重症肌无力患者,分为治疗前(病例组)和治疗后(治疗组),并纳入30名健康志愿者(对照组)。其中,治疗组采用加味补中益气汤(MBZYQD)治疗,比较治疗前(病例组)、治疗后(治疗组)和健康志愿者(对照组)血液中乙酰胆碱受体(AChR)、肌肉特异性激酶(Musk)和肌联蛋白(Titin)等抗体水平以及肠道微生物群情况。结果显示,MBZYQD治疗后,MG患者的AChR、MuSK和Titin抗体水平以及白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)和白细胞介素-22(IL-22)炎症因子水平显著降低,几乎恢复到健康水平。此外,MBZYQD治疗后,MG患者肠道微生物的多样性、结构和功能也恢复到健康水平。在门水平上,病例组变形菌门的相对丰度显著增加,与对照组相比,拟杆菌门的相对丰度显著降低,治疗组变形菌门和拟杆菌门的相对丰度与对照组相似。在属水平上,病例组[此处原文缺失属名]的相对丰度显著增加,[此处原文缺失属名]的相对丰度显著降低,治疗组[此处原文缺失属名]和[此处原文缺失属名]的相对丰度与对照组相似。此外,病例组中氟苯甲酸降解途径(KO00364)显著增加,而治疗组该途径显著降低。综上所述,MBZYQD可通过调节肠道微生物群的多样性、结构和功能来改善宿主免疫功能,从而治疗重症肌无力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/1a434e2d37b8/fmicb-13-1082565-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/98f27f2b7fab/fmicb-13-1082565-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/7595d391058f/fmicb-13-1082565-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/d9d577b60828/fmicb-13-1082565-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/1f82e0dc15b6/fmicb-13-1082565-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/1a434e2d37b8/fmicb-13-1082565-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/98f27f2b7fab/fmicb-13-1082565-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/7595d391058f/fmicb-13-1082565-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/d9d577b60828/fmicb-13-1082565-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/1f82e0dc15b6/fmicb-13-1082565-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fed5/9852828/1a434e2d37b8/fmicb-13-1082565-g005.jpg

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