Modulation of choline and lactate metabolism by basic fibroblast growth factor mitigates neuroinflammation in type 2 diabetes: Insights from 1H-NMR metabolomics analysis

doi:10.1016/j.neuropharm.2024.110049

科研成果详情

题名	Modulation of choline and lactate metabolism by basic fibroblast growth factor mitigates neuroinflammation in type 2 diabetes: Insights from 1H-NMR metabolomics analysis
作者	Wu, Yali1,3; Wang, Xinyi 1,3; Zhang, Wenli 1,3; Fu, Jun 2; Jiang, Kaidong1,3; Shen, Yuying1,3; Li, Chen 1,3; Gao, Hongchang1,2,3
发表日期	2024-10-01
发表期刊	Neuropharmacology 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Type 2 diabetes bFGF Inflammation NF -KB 1 H-NMR metabolomics
其他关键词	CHAIN AMINO-ACIDS ; CREATINE SUPPLEMENTATION ; INFLAMMATION ; MONOHYDRATE ; PROTECTS ; SURVIVAL ; SYSTEM ; MODEL ; LINK
摘要	Background: Type 2 diabetes (T2D), a chronic metabolic disease, occurs brain dysfunction accompanied with neuroinflammation and metabolic disorders. The neuroprotective effects of the basic fibroblast growth factor (bFGF) have been well studied. However, the mechanism underlying the anti-inflammatory effects of bFGF remains elusive. Methods: In this study, db/db mice were employed as an in vivo model, while high glucose (HG)-induced SY5Y cells and LPS-induced BV2 cells were used as in vitro models. Liposomal transfection of MyD88 DNA plasmid was used for MyD88-NF-KB pathway studies. And western blotting, flow cytometry and qPCR were employed. 1HNMR metabolomics was used to find out metabolic changes. Results: bFGF mitigated neuroinflammatory and metabolic disorders by inhibiting cortical inflammatory factor secretion and microglia hyperactivation in the cortex of db/db mice. Also, bFGF was observed to inhibit the MyD88-NF-KB pathway in high glucose (HG)-induced SY5Y cells and LPS-induced BV2 cells in in vitro experiments. Moreover, the 1H-NMR metabolomics results showed that discernible disparities between the cortical metabolic profiles of bFGF-treated db/db mice and their untreated counterparts. Notably, excessive lactate and choline deficiency attenuated the anti-inflammatory protective effect of bFGF in SY5Y cells. Conclusion: bFGF ameliorates neuroinflammation in db/db mice by inhibiting the MyD88-NF-kB pathway. This finding expands the potential application of bFGF in the treatment of neuroinflammation-related cognitive dysfunction.
资助项目	National Natural Science of China [22274115]
出版者	PERGAMON-ELSEVIER SCIENCE LTD
ISSN	0028-3908
EISSN	1873-7064
卷号	257
DOI	10.1016/j.neuropharm.2024.110049
页数	10
WOS类目	Neurosciences ; Pharmacology & Pharmacy
WOS研究方向	Neurosciences & Neurology ; Pharmacology & Pharmacy
WOS记录号	WOS:001261799300001
收录类别	SCIE ; SCOPUS ; PUBMED
URL	查看原文
PubMed ID	38901641
SCOPUSEID	2-s2.0-85196805876
通讯作者地址	[Li, Chen;Gao, Hongchang]Wenzhou Med Univ, Chashan Univ Town, Wenzhou 325035, Peoples R China.
Scopus学科分类	Pharmacology;Cellular and Molecular Neuroscience
SCOPUS_ID	SCOPUS_ID:85196805876
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/215289
专题	附属第二医院_核磁共振室温州医科大学
通讯作者	Li, Chen; Gao, Hongchang
作者单位	1.Wenzhou Med Univ, Inst Metabon & Med NMR, Sch Pharmaceut Sci, Oujiang Lab,Zhejiang Lab Regenerat Med Vis & Brain, Wenzhou 325035, Peoples R China; 2.Wenzhou Med Univ, Innocat Acad Testing Technol, Wenzhou, Peoples R China; 3.Key Lab Efficacy Evaluat Tradit Chinese Med & Ence, Wenzhou 325035, Peoples R China
第一作者单位	附属第二医院_核磁共振室
通讯作者单位	温州医科大学
第一作者的第一单位	附属第二医院_核磁共振室
推荐引用方式 GB/T 7714	Wu, Yali,Wang, Xinyi,Zhang, Wenli,et al. Modulation of choline and lactate metabolism by basic fibroblast growth factor mitigates neuroinflammation in type 2 diabetes: Insights from 1H-NMR metabolomics analysis[J]. Neuropharmacology,2024,257.
APA	Wu, Yali., Wang, Xinyi., Zhang, Wenli., Fu, Jun., Jiang, Kaidong., ... & Gao, Hongchang. (2024). Modulation of choline and lactate metabolism by basic fibroblast growth factor mitigates neuroinflammation in type 2 diabetes: Insights from 1H-NMR metabolomics analysis. Neuropharmacology, 257.
MLA	Wu, Yali,et al."Modulation of choline and lactate metabolism by basic fibroblast growth factor mitigates neuroinflammation in type 2 diabetes: Insights from 1H-NMR metabolomics analysis".Neuropharmacology 257(2024).