Related Experiment Video
Updated: Mar 16, 2026
Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
Published on: April 18, 2025
The Protective Effect of Low-Dose Ethanol on Myocardial Fibrosis through Downregulating the JNK Signaling Pathway in
Ying Yu1, Xian-Jie Jia2, Wei-Ping Zhang1
1Department of Physiology, Bengbu Medical College, 2600 Dong Hai Avenue, Bengbu 233030, China.
Abstract:
Objective. To investigate the effects of low dose ethanol feeding in diabetic rats and analyze its underlying mechanisms. Methods. Male Sprague-Dawley rats were divided into 4 groups: control (Con), diabetes at 4 weeks (DM4W), diabetes at 8 weeks (DM8W), and EtOH + DM8W. After 8 weeks, hemodynamic parameters were recorded and heart weight/body weight (H/B) and hydroxyproline (Hp) content in myocardium were measured. Morphology of collagen in myocardial tissue was observed with Masson's trichrome staining method and collagen volume fraction (CVF) was analysed. The mRNA expression of ALDH2 was assessed with Real-Time PCR. The protein expressions of p-JNK and JNK were evaluated using western blot. Results. In contrast to Con group, there was no difference in hemodynamic parameters in DM4W group, but mean arterial pressure and heart rate were decreased in DM8W group, and the ratios of H/B, Hp, and CVF were markedly increased. ALDH2 mRNA expression was decreased, while the ratio of p-JNK/JNK were increased. Compared with DM8W group, the above indexes were improved in EtOH + DM8W group. Conclusion. With low dose ethanol intervention, enhanced ALDH2 expression can antagonize the happening of myocardial fibrosis in diabetic rats, which may be relevant with downregulating the JNK pathway.
Insights
Low-dose ethanol feeding improved cardiac function in diabetic rats by enhancing ALDH2 expression and downregulating the JNK pathway, mitigating myocardial fibrosis.
Area of Science:
- Cardiovascular Research
- Diabetology
- Pharmacology
Background:
- Diabetic cardiomyopathy is a significant complication of diabetes mellitus.
- Myocardial fibrosis and altered cardiac function are key pathological features.
- The role of low-dose ethanol in mitigating diabetic cardiac complications is not well understood.
Purpose of the Study:
- To investigate the protective effects of low-dose ethanol on diabetic cardiomyopathy in rats.
- To elucidate the underlying molecular mechanisms involving ALDH2 and JNK signaling.
Main Methods:
- Male Sprague-Dawley rats were induced with diabetes and divided into control, diabetic (4 and 8 weeks), and ethanol-treated diabetic groups.
- Hemodynamic parameters, heart/body weight ratio, myocardial hydroxyproline content, and collagen volume fraction were assessed.
- ALDH2 mRNA expression and JNK pathway activation (p-JNK/JNK ratio) were analyzed.
Main Results:
- Diabetic rats exhibited decreased cardiac function, increased heart weight/body weight ratio, elevated myocardial hydroxyproline and collagen volume fraction, decreased ALDH2 mRNA, and increased p-JNK/JNK ratio.
- Low-dose ethanol intervention improved hemodynamic parameters and reduced myocardial fibrosis markers.
- Ethanol treatment upregulated ALDH2 expression and downregulated the p-JNK/JNK ratio.
Conclusions:
- Low-dose ethanol exerts a protective effect against diabetic myocardial fibrosis.
- Enhanced ALDH2 expression and JNK pathway modulation are key mechanisms underlying ethanol's cardioprotective effects in diabetes.
