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Integrated Analysis of Gut Microbiota, Serum Metabolomics, and Proteomics Reveals Novel Associations With Clinical Symptoms in Patients With Cerebral Infarction

ABSTRACT: Cerebral infarction (CI) is a major cause of adult disability and mortality worldwide. Mounting evidence supports the critical role of the gut–brain axis in cerebrovascular disease progression. This study aimed to characterize the alterations in gut microbiota, serum metabolome, and serum proteome in patients with CI, and to identify multi-omics signatures associated with clinical symptoms. A total of 20 CI patients and 20 healthy controls (HC) were enrolled. Fecal microbiota was profiled using 16S rRNA gene high-throughput sequencing. Serum metabolomics and proteomics were analyzed using ultra-high-performance liquid chromatography–tandem mass spectrometry (UPLC–MS/MS) and data-independent acquisition (DIA) proteomics, respectively. Spearman correlation and multi-omics integration were applied to explore the associations among microbiota, metabolites, proteins, and clinical indicators.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS14356 | MetaboLights | 2026-05-08

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS14356_LC-MS_negative_reverse-phase.txt	Txt
	a_MTBLS14356_LC-MS_positive_reverse-phase.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS14356_LC-MS_negative_reverse-phase_v2_maf.tsv	Tabular
	m_MTBLS14356_LC-MS_positive_reverse-phase_v2_maf.tsv	Tabular

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Project description:Background and Objective: Cerebral infarction (CI) is a severe neurological disorder caused by localized disruption of blood supply to brain tissue, leading to high rates of disability and mortality. Circular RNAs (circRNAs), highly expressed in the brain, have been identified as potential therapeutic targets for CI. Although acupuncture has been shown to promote neurological recovery, the precise molecular mechanisms, particularly the role of circRNAs in regulating angiogenesis, remain insufficiently understood. This study is the first to demonstrate that electroacupuncture (EA) promotes angiogenesis by regulating the circRNA_011971/miR-196c-5p/ARL13B axis, enhancing the proliferation and migration of brain microvascular endothelial cells (BMECs), and accelerating angiogenesis. These findings provide new insights into the molecular mechanisms of acupuncture treatment for CI and identify potential therapeutic targets. Methods: Male Wistar rats were used to establish a cerebral infarction model via middle cerebral artery occlusion (MCAO). The rats were divided into a model group, an EA treatment group, and a control group. Immediately after MCAO induction, the EA group received acupuncture at the GV26 acupoint. Neurological deficits were assessed using the modified Neurological Severity Score (mNSS), and infarct volumes were measured using TTC staining. Immunofluorescence double staining was performed to detect angiogenesis markers CD31 and Ki67 in the peri-infarct area. CircRNA expression profiles in brain tissue were obtained through circRNA microarray analysis, and key circRNAs were validated via qRT-PCR and fluorescence in situ hybridization (FISH). In BMECs, circRNA_011971 knockdown was achieved using shRNA, and its biological functions were assessed through CCK8, wound healing, and transwell assays. The expression levels of Arl13b, VEGFA, and VEGFR2 were measured using qRT-PCR and Western blot after circRNA_011971 knockdown or overexpression. Molecular interactions among circRNA_011971, miR-196c-5p, and ARL13B were explored using dual-luciferase reporter assays, RNA immunoprecipitation (RIP), and co-immunoprecipitation (Co-IP). Results: Compared to the untreated group, the EA group exhibited significantly smaller infarct volumes, suggesting immediate EA treatment at GV26 following infarction can effectively limit infarct progression. Immunofluorescence analysis revealed a marked increase in the co-expression of CD31 and Ki67 in the peri-infarct region of the EA-treated rats, indicating enhanced angiogenesis. CircRNA microarray analysis showed that circRNA_011971 was significantly upregulated following ischemia and downregulated after EA treatment. In BMECs, circRNA_011971 knockdown inhibited cell proliferation, migration, and invasion, whereas its overexpression promoted these processes. Further mechanistic studies revealed that EA downregulated rno_circ_011971 expression, lifting its inhibition on miR-196c-5p and activating the ARL13B/VEGF signaling pathway, thereby significantly promoting angiogenesis. This study discover a molecular mechanism by which EA regulates post-CI angiogenesis through the circRNA/miRNA axis for the first time, offering new potential targets for acupuncture therapy. Conclusion: EA improves neurological function, reduces infarct size, and promotes angiogenesis, potentially through regulating of VEGFR via the rno_circ_011971/miR-196c-5p/ARL13B axis.

Project description:Background The restoration of cerebrovascular regulation and improvement of cerebral blood flow in ischaemic regions are crucial for improving the clinical prognosis after stroke. An-Gong-Niu-Huang-Wan (AGNHW) is a famous traditional compound Chinese medicine that has been used for over 220 years to treat acute ischaemic stroke; however, its role in the regulation of cerebral blood flow is still unclear. The aim of the present study was to investigate the regulatory effect of AGNHW on cerebral blood flow and microcirculation after ischaemic stroke and to elucidate the underlying mechanisms involved. Methods Male C57BL/6 mice were subjected to distal middle cerebral artery occlusion (dMCAO) and randomly assigned to the sham, MCAO, or AGNHW groups. AGNHW was administered intragastrically 1 h after dMCAO. The rotarod test was utilized to evaluate behavioural function; TTC was used to determine the infarct volume; and ischaemic injury was assessed by detecting brain levels of SOD, MDA and NO. Then, cortical perfusion and acetazolamideinduced cerebrovascular reactivity were assessed using laser speckle contrast imaging, and the velocity and flux of red blood cells in cortical capillaries were detected using two-photon laser scanning microscopy. In addition, we employed RNA-Seq to identify variations in gene expression profiles and assessed endothelium-dependent changes in microcirculatory dysfunction by measuring vasoactive mediator levels. Results AGNHW significantly increased cerebral blood flow, reduced the infarct volume, and promoted functional recovery after cerebral ischaemia. AGNHW increased the velocity and flux of red blood cells in capillaries and improved cerebrovascular reactivity in the ischaemic cortex. Furthermore, AGNHW regulated endotheliumdependent microcirculation, as evidenced by decreases in the expression of endothelins (Edn1, Edn3 and Ednrb) and the ratios of brain and serum TXB2/6-keto-PGF1α and ET-1/CGRP. Conclusions AGNHW improved cerebral hypoperfusion, regulated cerebrovascular reactivity and attenuated microcirculatory dysfunction within the ischaemic cortex after stroke. This outstanding effect was achieved by modulatingthe expression of genes related to vascular endothelial cell function and regulating endothelium-dependent vasoactive mediators.

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Integrated Analysis of Gut Microbiota, Serum Metabolomics, and Proteomics Reveals Novel Associations With Clinical Symptoms in Patients With Cerebral Infarction

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