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[Berberine ameliorates coronary artery endothelial cell injury in Kawasaki disease through complement and coagulation
Jin-Wen Liao1, Xin Guo1, Bo Liang
1Department of Pediatrics, Third People's Hospital of Longgang District of Shenzhen, Shenzhen, Guangdong 518020, China.
Insights
Berberine (BBR) treatment may protect against coronary endothelial cell injury in Kawasaki disease (KD) by modulating the complement and coagulation cascade. Key proteins like C1QC, KNG1, C1S, and C4BPA may serve as biomarkers for BBR efficacy in KD.
Area of Science:
- Proteomics
- Molecular Biology
- Immunology
Context:
- Kawasaki disease (KD) poses a significant risk of coronary artery aneurysms due to endothelial cell injury.
- The complement and coagulation cascades are implicated in KD pathogenesis.
- Berberine (BBR) is a natural compound with potential therapeutic properties.
Purpose:
- To investigate the therapeutic effect of berberine (BBR) on coronary endothelial cell injury in Kawasaki disease (KD).
- To explore the underlying molecular mechanisms involving the complement and coagulation cascade.
- To identify potential protein biomarkers for BBR treatment in KD.
Summary:
- Differential protein expression analysis identified 518 proteins between KD and healthy control cells, and 422 between BBR-treated and KD cells.
- Bioinformatics analysis revealed enrichment in complement and coagulation cascade pathways in KD, which were also modulated by BBR treatment.
- Western blot confirmed increased expression of C1QC, KNG1, C1S, and C4BPA in KD, with decreased expression following BBR treatment.
Impact:
- This study elucidates the role of BBR in mitigating KD-induced endothelial injury via complement and coagulation pathways.
- Identified C1QC, KNG1, C1S, and C4BPA as potential biomarkers for monitoring BBR treatment effectiveness in KD.
- Provides a basis for developing novel therapeutic strategies targeting these pathways in KD management.
Objectives:
To explore the role of berberine (BBR) in ameliorating coronary endothelial cell injury in Kawasaki disease (KD) by regulating the complement and coagulation cascade.
Methods:
Human coronary artery endothelial cells (HCAEC) were divided into a healthy control group, a KD group, and a BBR treatment group (n=3 for each group). The healthy control group and KD group were supplemented with 15% serum from healthy children and KD patients, respectively, while the BBR treatment group received 15% serum from KD patients followed by the addition of 20 mmol/L BBR. Differential protein expression was analyzed and identified using isobaric tags for relative and absolute quantitation technology and liquid chromatography-tandem mass spectrometry, followed by GO functional enrichment analysis and KEGG signaling pathway enrichment analysis of the differential proteins. Western blot was used to detect differential protein expression.
Results:
A total of 518 differential proteins were identified between the KD group and the healthy control group (300 upregulated proteins and 218 downregulated proteins). A total of 422 differential proteins were identified between the BBR treatment group and the KD group (221 upregulated proteins and 201 downregulated proteins). Bioinformatics analysis showed that compared to the healthy control group, the differential proteins in the KD group were enriched in the complement and coagulation cascade and ribosome biogenesis in eukaryotes. Compared to the KD group, the differential proteins in the BBR treatment group were also enriched in the complement and coagulation cascade and ribosome biogenesis in eukaryotes. Western blot results indicated that compared to the healthy control group, the expression of complement C1q subcomponent subunit C (C1QC), kininogen-1 (KNG1), complement C1s subcomponent (C1S), and C4b-binding protein alpha chain (C4BPA) was increased in the KD group (P<0.05). Compared to the KD group, the expression of KNG1, C1S, C1QC, and C4BPA was decreased in the BBR treatment group (P<0.05).
Conclusions:
The complement and coagulation cascade may be involved in the regulation of BBR treatment for coronary injury in KD, and C1QC, KNG1, C1S, and C4BPA may serve as biomarkers for this treatment.
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