Berberine protects Kawasaki disease-induced human coronary artery endothelial cells dysfunction by inhibiting of oxidative and endoplasmic reticulum stress

Xu, Minhui; Qi, Qi; Men, Lina; Wang, Shushui; Li, Meng; Xiao, Min; Chen, Xiaozhou; Wang, Sheng; Wang, Guobing; Jia, Hongling; Liu, Cong

doi:10.1016/j.vph.2020.106660

Cited by 36 publications

(33 citation statements)

References 22 publications

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“…KD is the leading cause of acquired heart disease in children, given its coronary artery complications [9,10], and there is still no effective therapy to prevent or treat the occurrence of coronary artery damage due to the limited information. It has been shown that coronary artery endothelial dysfunction plays an important role in the development of coronary artery damage under KD condition [11,6]. Therefore, it is meaningful to gure out the changes in endothelial cells with or without KD condition, which might provide novel indicators and potential therapeutic targets for KD.…”

Section: Discussionmentioning

confidence: 99%

“…Endothelial cells play an indispensable role in maintaining the normal functions of vessels. And dysfunction or in ammatory activation of coronary artery endothelial cells lead to the disruption of endothelial cell homeostasis, which are the initiating factors for the damage of coronary artery in patients with KD [6][7][8].Therefore, a better understanding of alterations in coronary artery endothelial cells underlying KD is required to develop targeted treatments. RNA-sequencing (RNAseq) has been widely used to analyze gene expression offering a cheap, e cient and high throughput method to investigate global gene expression patterns.…”

Section: Introductionmentioning

confidence: 99%

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Expression profile analysis of Differentially Expressed Genes in Human Coronary Artery Endothelial Cells Induced by Serum from Kawasaki Disease: A preliminary study

Fan

Xiao

et al. 2020

Preprint

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Background: Kawasaki disease (KD) leads to coronary artery damage and the etiology of KD is unknown. The present study was designed to explore the differentially expressed genes (DEGs) in KD serum-induced human coronary artery endothelial cells (HCAECs) by RNA-sequence (RNA-seq). Methods: HCAECs were stimulated with serum (15% (v/v)), which were collected from 20 healthy children and 20 KD patients, for 24 hours. DEGs were then detected and analyzed by RNA-seq and bioinformatics analysis. Results: The expression of SMAD1, SMAD6, CD34, CXCL1, PITX2, and APLN was validated by qPCR. 102 genes, 59 up-regulated and 43 down-regulated genes, were significantly differentially expressed in KD groups. GO enrichment analysis showed that DEGs were enriched in cellular response to cytokines, cytokine-mediated signaling pathway, and regulation of immune cells migration and chemotaxis. KEGG signaling pathway analysis showed that DEGs were mainly involved in cytokine−cytokine receptor interaction, chemokine signaling pathway, and TGF−β signaling pathway. Besides, the mRNA expression levels of SMAD1, SMAD6, CD34, CXCL1, and APLN in the KD group were signiﬁcantly up-regulated compared with the normal group, whilePITX2 was significantly down-regulated. Conclusion: 102 DEGs in KD serum-induced HCAECs were identified, and six new targets were proposed as potential indicators of KD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression profile analysis of Differentially Expressed Genes in Human Coronary Artery Endothelial Cells Induced by Serum from Kawasaki Disease: A preliminary study

Fan

Xiao

et al. 2020

Preprint

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“…Traditional Chinese medicine is suitable for treating diseases with complex mechanisms and, because of its multiple curative effect and small side effects. The effects of BBR on KD in clinical practice were tested based on some previous ndings regarding this topic [13]. The present study can be considered the rst clinical trial to evaluate the effect of BBR in patients with KD.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, another examination con rmed that BBR protects KD-induced human coronary artery endothelial cells dysfunction by inhibiting oxidative and endoplasmic reticulum stress [13].…”

Section: Introductionmentioning

confidence: 97%

Utilizing Network Pharmacology to Explore the Possible Mechanism of CoptidisRhizoma in Kawasaki Disease

Fan

Guo

2020

Preprint

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Background: Kawasaki disease (KD) isan acute self-limiting systemic vasculitis.In this study, a randomized controlled trial regarding berberine (main component of CoptidisRhizoma) function in treating KD was carried out and possible pharmacological mechanisms of CoptidisRhizoma (CR) on Kawasaki disease therapy were investigated using an integrated network pharmacology approach.Results: The BBR group was able to reduce the values of CRP, NLR and PLR significantly. Also, the effect of BBR improved the resistance rate of intravenous injection of gamma globulin significantly. In total, 9 compounds and 369 relative drug targets were collected from TCMSP, SWISS, SEA and STITCH database and 624 KD target genes were collected in DisGeNET, DrugBank and GeneCards database. The network analysis revealed that 41 targets might be the therapeutic targets of CR on KD, among which ATK1, RELA, SRC, CASP3 and MTOR ranked in top 5. Gene ontology enrichment analysis revealed that the reaction to bacteria-derived molecules and to lipopolysaccharide and the apoptosis process were the key biological procedures for CR treating KD. The KEGG pathway enrichment analysis pointed out that the four signaling pathways closely related to CR treating KD including age-rage signaling pathway, fluid shear stress and atherosclerosis, TNF signaling pathway and Toll-like receptor signaling pathway in diabetic complications.Conclusion: We concluded that the introduction of routine treatment combined with BBR in treating KD has advantages than routine treatment and can be considered as a preferred approach in KD. Network pharmacology showed that CR exerted the effect of prevention KD by regulating multi-targets and multi-components.

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“…In this study, we choose HCAECs as the tool cells, the main considerations are: (1) Coronary artery endothelial injury is the early stage of the development of CHD. (2) HCAECs are widely used as tool cells to explore oxidative damage including endothelial dysfunction caused by ox-LDL (24)(25)(26). (3) The primary HCAECs ox-LDL injury model used in this manuscript is closer to the pathological conditions of CHD.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA ENST00000609755.1 Confers Protection Against Early oxLDL-Induced Coronary Heart Disease

Sun

Huang

Wan

et al. 2021

Front. Cardiovasc. Med.

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Background: This study investigated the association between long non-coding RNAs (lncRNAs) and coronary heart disease (CHD) and further elucidated the potential biological roles of lncRNAs in CHD pathogenesis.Methods: A case-control study (590 patients and 590 controls) was conducted from February 2017 and March 2019 in Fuzhou, China. Environmental factors were investigated using questionnaires and physical examinations. Five representative lncRNAs were screened using lncRNA microarray (peripheral blood in 5 cases and 5 controls) and further verified by quantitative real-time polymerase chain reaction (peripheral blood leukocyte in 100 cases and 100 controls). Oxidized low-density lipoprotein (oxLDL) was used to induce a human coronary artery endothelial cell (HCAECs) injury model, and loss of function was used to elucidate the role of lncRNA ENST00000609755.1 (lnc-MICALL2-2) in oxLDL-induced HCAECs injury.Results: A total of 320 lncRNAs were found dysregulated in CHD patients (fold change> 2, p < 0.05). The results of a discovery microarray, population verification and HCAEC experiments suggested the lnc-MICALL2-2 is upregulated in CHD subjects and in an oxLDL-induced HCAECs injury model. Conversely, lnc-MICALL2-2 inhibition in vitro attenuated the effects of oxLDL on HCAECs morphology, proliferation, and apoptosis.Conclusion: Elevated expression of lnc-MICALL2-2 is an independent risk factor for CHD, and knockdown subsequently confers protection against early pathological processes of oxLDL-induced CHD.

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Berberine protects Kawasaki disease-induced human coronary artery endothelial cells dysfunction by inhibiting of oxidative and endoplasmic reticulum stress

Cited by 36 publications

References 22 publications

Expression profile analysis of Differentially Expressed Genes in Human Coronary Artery Endothelial Cells Induced by Serum from Kawasaki Disease: A preliminary study

Expression profile analysis of Differentially Expressed Genes in Human Coronary Artery Endothelial Cells Induced by Serum from Kawasaki Disease: A preliminary study

Utilizing Network Pharmacology to Explore the Possible Mechanism of CoptidisRhizoma in Kawasaki Disease

Knockdown of lncRNA ENST00000609755.1 Confers Protection Against Early oxLDL-Induced Coronary Heart Disease

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