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Astragaloside IV Ameliorates Diabetic Cardiomyopathy by Suppressing the GNG2/MRAS-ERK Signaling Pathway
Ying Dong1, Yidi Ma2, Shi-Jan Liu3
1The First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, People's Republic of China.
Objective:
This study aims to investigate the mechanism of AGS-IV in treating diabetic cardiomyopathy (DCM) by establishing animal and cellular models of the disease.
Methods:
A DCM rat model was established by feeding a high-fat diet combined with streptozotocin (STZ) injection, and a DCM cell model was created through glucose induction. In model rats, the cardiac weight-to-body weight ratio, the left ventricular weight-to-heart weight ratio, and ventricular wall thickness were measured. ELISA was used to detect Collagen1 and MMP-2 levels in myocardial tissue, serum, and cultured cells. The mRNA levels of GNG2, MRAS, and ERK in myocardial tissue and cultured cells were measured using RT-PCR.
Results:
In vivo, experiments demonstrated that AGS-IV effectively reduced the cardiac weight-to-body weight ratio, left ventricular weight-to-heart weight ratio, and ventricular wall thickness in DCM rat models. It also decreased Collagen I levels in myocardial tissue and MMP-2 levels in serum, accompanied by downregulated mRNA expression of GNG2, MRAS, and ERK in myocardial tissue. In vitro, AGS-IV significantly reduced Collagen I and MMP-2 levels in DCM cell models and downregulated GNG2, MRAS, and ERK mRNA expression.
Conclusion:
AGS-IV exerts therapeutic effects on DCM by regulating the GNG2/MRAS-ERK signaling pathway.
Insights
AGS-IV effectively treats diabetic cardiomyopathy (DCM) by reducing cardiac hypertrophy and fibrosis. This study reveals AGS-IV regulates the GNG2/MRAS-ERK pathway, offering a new therapeutic strategy for DCM.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Pharmacology
Background:
- Diabetic cardiomyopathy (DCM) is a serious complication of diabetes mellitus, characterized by cardiac dysfunction.
- Understanding the molecular mechanisms underlying DCM is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the therapeutic mechanism of AGS-IV in treating diabetic cardiomyopathy (DCM).
- To establish and utilize animal and cellular models of DCM for mechanistic studies.
Main Methods:
- Diabetic cardiomyopathy rat models were induced using a high-fat diet and streptozotocin (STZ).
- Cellular models of DCM were established via glucose induction.
- Cardiac hypertrophy markers, collagen levels (Collagen I), MMP-2, and mRNA expression of GNG2, MRAS, and ERK were assessed using ELISA and RT-PCR.
Main Results:
- AGS-IV treatment significantly reduced cardiac hypertrophy indicators (cardiac weight-to-body weight ratio, left ventricular weight-to-heart weight ratio, ventricular wall thickness) in DCM rat models.
- AGS-IV decreased Collagen I and MMP-2 levels in both in vivo and in vitro DCM models.
- Downregulation of GNG2, MRAS, and ERK mRNA expression was observed in myocardial tissue and cells treated with AGS-IV.
Conclusions:
- AGS-IV demonstrates significant therapeutic effects on diabetic cardiomyopathy.
- The mechanism involves the regulation of the GNG2/MRAS-ERK signaling pathway by AGS-IV.
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