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Exploring the mechanisms of baicalin in diabetic cardiomyopathy: Insights from network pharmacology and experimental
Xuyong Zhao1, Lina Xie1, Ning Zhu1
1Department of Cardiology, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, Zhejiang 32500, P.R. China.
Insights
Baicalin protects against diabetic cardiomyopathy by inhibiting inflammation, pyroptosis, and fibrosis. It targets protein tyrosine phosphatase non-receptor type 22 (PTPN22) and tumor necrosis factor (TNF) signaling pathways.
Area of Science:
- Cardiovascular Research
- Molecular Pharmacology
- Diabetology
Background:
- Diabetic cardiomyopathy (DCM) poses a significant threat to cardiovascular health.
- Baicalin demonstrates cardioprotective effects, but its mechanisms in DCM are not fully understood.
Purpose of the Study:
- To elucidate the molecular mechanisms by which baicalin ameliorates DCM.
- To identify baicalin's specific molecular targets and pathways involved in DCM treatment.
Main Methods:
- Network pharmacology and molecular docking identified baicalin's targets.
- In vitro studies using H9c2 cells assessed baicalin's effects on high-glucose induced injury.
- Echocardiography, RT-PCR, ELISA, histopathology, immunofluorescence, and western blotting were employed.
Main Results:
- Baicalin alleviated high-glucose induced injury by inhibiting fibrotic markers, inflammation, and pyroptosis.
- Protein tyrosine phosphatase non-receptor type 22 (PTPN22) and tumor necrosis factor (TNF) were identified as key targets with strong binding affinity.
- Baicalin suppressed HG-induced pyroptosis, inflammation, and fibrosis by inhibiting TNF-α and PTPN22 signaling.
Conclusions:
- Baicalin exerts therapeutic effects in DCM by targeting PTPN22 and TNF-α.
- This study provides insights into baicalin's mechanisms and potential as a therapeutic agent for DCM.
Abstract:
Baicalin has protective effects against a range of cardiovascular conditions, such as myocardial ischemia-reperfusion injury, cardiac dysfunction, and apoptosis in cardiomyocytes. However, the underlying protective mechanisms in diabetic cardiomyopathy (DCM) remain unclear. The present study aimed to investigate the specific molecular mechanism activated by baicalin to ameliorate DCM. The effects of baicalin were investigated in vitro and its potential targets and pathways were identified using network pharmacology, molecular docking, echocardiography, reverse transcription PCR, ELISA, histopathology, immunofluorescence staining and western blotting. Baicalin significantly alleviated high-glucose (HG)-induced injury in H9c2 cells by inhibiting fibrotic markers, inflammatory factors and pyroptosis. Moreover, protein tyrosine phosphatase non-receptor type 22 (PTPN22) and tumor necrosis factor (TNF) were identified as crucial targets for baicalin. Molecular docking indicated that baicalin exhibited a strong binding affinity for PTPN22 and TNF. Baicalin successfully suppressed HG-induced pyroptosis, inflammation and fibrotic markers in addition to inhibiting the activation of TNF-α and PTPN22 signaling pathways. In addition, PTPN22-small interfering RNA treatment modulated pyroptosis in vitro. The present study offers insight into the key therapeutic mechanisms activated by baicalin, and its potential therapeutic targets, PTPN22 and TNF-α.