Related Experiment Video
Updated: Feb 6, 2026

Ultrasound-Guided Induced Pluripotent Stem Cell-Derived Cardiomyocyte Implantation in Myocardial Infarcted Mice
Published on: March 30, 2022
Fluvastatin inhibits cardiomyocyte apoptosis after myocardial infarction through Toll pathway
Lili Jia1,2, Liang Wang3, Wenxue Liu4
1Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China.
Abstract:
The present study intended to investigate the effect of fluvastatin on cardiomyocyte apoptosis after myocardial infarction in rats. Eighty myocardial infarction rat models were established and randomly divided into 4 groups (n=20): experimental group (n=20) was given fluvastatin treatment; sham operation group (n=20) and normal control group (n=20) were given saline. The dose of fluvastatin was 20 mg/(kg·d), and irrigation gavage was given for 1 week. Western blot analysis and reverse transcription-quantitative PCR (RT-qPCR) were used to detect the expression of TLR4 mRNA and protein in cardiomyocytes. TUNEL method was used to detect the apoptosis of cardiomyocytes. After fluvastatin treatment for 1 week, RT-qPCR found that compared with myocardial infarction group, the TLR4 mRNA expression of fluvastatin treatment group and normal control group was significantly increased, and the differences between groups were a statistically significant difference (P<0.05). Western blot analysis showed that compared with the myocardial infarction group, the expression of TLR4 protein in normal control group, sham operation group and fluvastatin treatment group were significantly decreased, and they all were statistically significant (P<0.05). TUNEL method found that compared with the myocardial infarction group, the fluvastatin treatment group could significantly reduce the apoptosis of cardiomyocytes (19.2±3.8%), and the difference was statistically significant (P<0.05). Fluvastatin can inhibit myocardial infarction and decrease cardiomyocyte apoptosis by increasing the expression of TLR4-like receptor.
Insights
Fluzastatin treatment significantly reduced cardiomyocyte apoptosis following myocardial infarction in rats. This effect was associated with changes in Toll-like receptor 4 (TLR4) expression, suggesting a protective role.
Area of Science:
- Cardiology
- Pharmacology
- Molecular Biology
Background:
- Myocardial infarction (MI) leads to cardiomyocyte apoptosis.
- Statins, like fluvastatin, are used to manage cardiovascular disease.
- The role of Toll-like receptor 4 (TLR4) in MI-induced apoptosis requires further investigation.
Purpose of the Study:
- To investigate the effect of fluvastatin on cardiomyocyte apoptosis in a rat model of myocardial infarction.
- To explore the potential mechanism involving Toll-like receptor 4 (TLR4) expression.
Main Methods:
- Establishment of rat models of myocardial infarction.
- Treatment with fluvastatin (20 mg/kg/day) for one week.
- Assessment of TLR4 mRNA and protein expression using RT-qPCR and Western blot.
- Detection of cardiomyocyte apoptosis via TUNEL assay.
Main Results:
- Fluvastatin treatment significantly reduced cardiomyocyte apoptosis (19.2±3.8%) compared to the MI group (P<0.05).
- RT-qPCR showed significantly increased TLR4 mRNA expression in the fluvastatin and normal control groups compared to the MI group (P<0.05).
- Western blot analysis revealed significantly decreased TLR4 protein expression in normal control, sham operation, and fluvastatin treatment groups compared to the MI group (P<0.05).
Conclusions:
- Fluvastatin demonstrates a cardioprotective effect by inhibiting cardiomyocyte apoptosis after myocardial infarction in rats.
- The mechanism may involve the modulation of Toll-like receptor 4 (TLR4) signaling pathways.
Related Concept Videos
Feedback Inhibition
Apoptosis
C4 Pathway and CAM
C4 Pathway
The C4 pathway is used by plants such as...
Enzyme Inhibition
Inhibition of Cdk Activity
Other Glycolytic Pathways

