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1.上海中医药大学附属光华医院风湿科(上海 200052)
2.上海交通大学医学院附属瑞金医院骨伤科(上海 200025)
3.山东中医药大学附属医院风湿科(山东 济南 250014)
4.上海交通大学医学院附属同仁医院康复科(上海 200336)
姜平,男,博士,主治医师,主要从事中医药防治风湿病的研究工作
何秉恒,住院医师;E-mail:hhebingheng@126.com
收稿:2024-10-29,
纸质出版:2026-01-10
移动端阅览
姜平,常岑,金晔华,等.基于转录组测序探索雷公藤甲素与雷藤舒对类风湿关节炎滑膜成纤维细胞调控机制的异同[J].上海中医药杂志,2026,60(1):32-40.
JIANG Ping,CHANG Cen,JIN Yehua,et al.Exploring similarities and differences in regulatory mechanisms of triptolide and (5R)‑5‑hydroxytriptolide on rheumatoid arthritis fibroblast‑like synoviocytes based on transcriptome sequencing[J].Shanghai Journal of Traditional Chinese Medicine,2026,60(1):32-40.
姜平,常岑,金晔华,等.基于转录组测序探索雷公藤甲素与雷藤舒对类风湿关节炎滑膜成纤维细胞调控机制的异同[J].上海中医药杂志,2026,60(1):32-40. DOI: 10.16305/j.1007-1334.2026.z20241029006.
JIANG Ping,CHANG Cen,JIN Yehua,et al.Exploring similarities and differences in regulatory mechanisms of triptolide and (5R)‑5‑hydroxytriptolide on rheumatoid arthritis fibroblast‑like synoviocytes based on transcriptome sequencing[J].Shanghai Journal of Traditional Chinese Medicine,2026,60(1):32-40. DOI: 10.16305/j.1007-1334.2026.z20241029006.
目的
2
通过转录组测序探索雷公藤甲素(TP)与雷藤舒(T8)调控类风湿关节炎(RA)滑膜成纤维细胞(FLS)的分子机制。
方法
2
使用TP与T8分别干预FLS株MH7A,24 h后收集细胞并进行转录组测序,并对测序结果进行生物信息学分析。
结果
2
TP调控的关键基因包括肿瘤坏死因子基因(
TNF
)、Toll样受体2基因
(TLR2)
、核因子κB抑制因子
α
基因(
NFKBIA
)、白细胞介素-6基因(
IL
-
6
)和白细胞介素-1β基因(
IL
-
1β
)等;这些基因主要涉及炎症反应、细胞对内毒素的反应以及内毒素介导的信号转导等生物过程;此外,相关的信号通路还包括NOD样受体(NLR)信号通路等。T8调控的关键基因包括
TNF
、
NFKBIA
、
IL
-
6
、
IL
-
4
和
IL
-
1β
等,主要涉及炎症反应、纤维蛋白溶解、血管生成的正向调节等生物过程以及IL-17等信号通路。
结论
2
TP和T8在调控RA-FLS的具体作用靶点和信号通路上具有部分共性和不同,这可为TP和T8在RA中的研究提供更多的数据支持,也为新型化合物T8在治疗RA方面的机制研究提供新见解。
Objective
2
To explore the molecular mechanisms by which triptolide (TP) and (5
R
)-5-hydroxytriptolide (T8) regulate fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA) using transcriptome sequencing.
Methods
2
The synovial fibroblast cell line MH7A was intervened with TP and T8 respectively. After 24 h, the cells were collected and transcriptome sequencing was performed, and the sequencing results were analyzed by bioinformatics.
Results
2
Key genes are regulated by TP included tumor necrosis factor (
TNF
), toll-like receptor 2 (
TLR2
), nuclear factor kappa B inhibitor alpha (
NFKBIA
), interleukin (
IL
)-6, and
IL
-
1β
. These genes are primarily involved in biological processes such as inflammatory response, cellular response to endotoxin, and endotoxin-mediated signal transduction. Relevant signaling pathways include NOD-like receptors (NLR) pathways. Key genes are regulated by T8 included
TNF
,
NFKBIA
,
IL
-
6
,
IL
-
4
, and
IL
-
1β
, associated with processes such as inflammatory response, positive regulation of fibrinolysis, and angiogenesis, as well as the IL-17 signaling pathway.
Conclusions
2
TP and T8 share some commonalities and differences in the specific targets and signaling pathways regulating RA-FLS. This provides additional data support for previous studies on TP and T8 in RA and offers new insights into the mechanism of T8 as a novel compound for RA treatment.
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