Related Experiment Video
Updated: Aug 6, 2025
Author Spotlight: Investigating the Underlying Mechanisms of Right Ventricular Failure in Pulmonary Hypertension
Published on: June 14, 2024
Baicalin inhibits pressure overload-induced cardiac hypertrophy by regulating the SIRT3-dependent signaling pathway
Yi Cai1, Shisheng Jiang1, Chaoming Huang1
1Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou 511436, China.
Insights
Baicalin, a plant flavonoid, effectively inhibits cardiac hypertrophy by activating the SIRT3/LKB1/AMPK pathway. This study demonstrates baicalin
Area of Science:
- Cardiovascular Biology
- Molecular Pharmacology
- Biochemistry
Background:
- Sirtuin 3 (SIRT3) is a key protective protein against cardiac hypertrophy, with its inhibition accelerating hypertrophy and overexpression preventing it.
- Baicalin, a flavonoid from Scutellaria baicalensis, exhibits cardioprotective properties against cardiac hypertrophy, but its molecular mechanisms remain unclear.
Purpose of the Study:
- To investigate the anti-hypertrophic effects of baicalin on cardiac hypertrophy.
- To elucidate the underlying molecular mechanisms of baicalin's action, particularly its interaction with the SIRT3 pathway.
Main Methods:
- Established mouse models of abdominal aortic constriction (AAC)-induced cardiac hypertrophy and angiotensin II (Ang II)-induced cardiomyocyte hypertrophy.
- Assessed cardiac hypertrophy by measuring hypertrophic gene expression and cell surface area.
- Utilized echocardiography for in vivo cardiac function assessment.
- Analyzed protein expression within the SIRT3-dependent pathway using Western blotting.
Main Results:
- Baicalin suppressed Ang II-induced increases in cell surface area and expression of cardiac hypertrophy markers (β-MHC, BNP, ANF).
- Baicalin treatment reduced the hypertrophic impact in AAC-induced cardiac hypertrophy models.
- Baicalin was found to regulate the SIRT3/LKB1/AMPK signaling pathway, thereby preventing cardiac hypertrophy.
- Baicalin upregulated SIRT3 protein expression by inhibiting proteasome activity and activating PSMB5.
Conclusions:
- Baicalin inhibits cardiac hypertrophy via the SIRT3-dependent signaling pathway, highlighting its therapeutic potential for cardiac hypertrophy and heart failure.
- This study provides foundational experimental evidence for the potential clinical application of baicalin and related compounds in managing cardiac conditions.
Background:
The conserved sirtuin protein sirtuin 3 (SIRT3) is a vital protective protein for cardiac hypertrophy. Inhibition of SIRT3 accelerated the development of heart hypertrophy. On the other hand, myocardial hypertrophy was prevented by overexpressing SIRT3. SIRT3 has been proposed as a potential therapeutic target for managing or averting heart hypertrophy. Baicalin, a flavonoid extracted from the Scutellaria baicalensis plant, has anti-cardiovascular properties, including protection against cardiac hypertrophy. However, the molecular mechanism of the anti-hypertrophic effect of baicalin is not well known.
Purpose:
In this study, we aim to investigate the effect of baicalin on cardiac hypertrophy and explored its underlying molecular mechanisms.
Study-Design/Methods:
Abdominal aortic constriction (AAC)-induced mouse cardiac hypertrophy and angiotensin II (Ang II)-induced cardiomyocyte hypertrophy models were established. After baicalin treatment, cardiac hypertrophy was monitored by detecting the expression of hypertrophic genes and cell surface area. Echocardiogram was performed to check the heart function in vivo. Moreover, the protein expression of the SIRT3-dependent pathway was detected by Western blotting.
Results:
In this work, we demonstrated that baicalin might suppress the cell surface area and the expression of the Ang II -induced myosin heavy chain β (β-MHC), brain natriuretic polypeptide (BNP), and atrial natriuretic factor (ANF). Additionally, it reduced the AAC rats' hypertrophic impact. We also found that baicalin prevents cardiac hypertrophy by regulating SIRT3/LKB1/AMPK signaling pathway. Moreover, we showed that baicalin upregulated the SIRT3 protein expression by inhibiting proteasome and by the activation of 20 S proteasome subunit beta type-5 (PSMB5).
Conclusion:
These results offer the first proof that baicalin inhibits cardiac hypertrophy due to its effect on the SIRT3-dependent signaling pathway, indicating its potential for treating cardiac hypertrophy and heart failure. The present study provides a preliminary experimental basis for the clinical application of baicalin and baicalin-like compounds.
More Related Videos
Related Concept Videos
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:22Heart Failure Drugs: β-Blockers
01:17Antihypertensive Drugs: Action of β1 Blockers
01:29Heart Failure II: Pathophysiology
01:31Adrenergic Antagonists: ɑ and β-Receptor Blockers
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers