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Effect of lingguizhugan decoction on myocardial nuclear factor kappa B protein expression in rats with chronic heart
Jinling Huang1, Liang Wang, Hui Shi
1Department of Integrated TCM and Western Medicine, Anhui University of Traditional Chinese Medicine, Hefei 230038, China. jinling6181@126.com
Insights
Lingguizhugan decoction (LGZGD) improves heart function and structure in rats with chronic heart failure (CHF). It works by inhibiting nuclear factor kappa B (NF-kappaB), a key factor in heart disease progression.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Traditional Chinese Medicine
Background:
- Chronic heart failure (CHF) is a complex condition characterized by cardiac structural and functional abnormalities.
- Nuclear factor kappa B (NF-kappaB) plays a critical role in the inflammatory pathways implicated in the pathogenesis of CHF.
Purpose of the Study:
- To evaluate the therapeutic effects of Lingguizhugan decoction (LGZGD) on cardiac structure and function in a rat model of CHF.
- To elucidate the underlying mechanism of LGZGD action by examining its impact on myocardial and plasma levels of NF-kappaB.
Main Methods:
- A rat model of CHF was established via coronary artery ligation.
- Rats were treated with varying doses of LGZGD or Captopril for 4 weeks.
- Hemodynamic indices, cardiac morphology, and NF-kappaB (mRNA, protein, plasma) levels were assessed.
Main Results:
- CHF rats exhibited significant cardiac dysfunction and structural changes, with elevated NF-kappaB expression.
- LGZGD and Captopril treatments improved hemodynamic parameters, cardiac structure, and survival rates.
- LGZGD significantly reduced both myocardial and plasma NF-kappaB levels in a dose-dependent manner.
Conclusions:
- Lingguizhugan decoction demonstrates significant efficacy in ameliorating cardiac dysfunction and structural remodeling in chronic heart failure.
- The cardioprotective effects of LGZGD are attributed to its potent inhibition of the NF-kappaB signaling pathway.
Objective:
To investigate the effect of Lingguizhugan decoction (LGZGD) on changes of cardiac structure and function, and its putative mechanism of action, by investigating mRNA and protein expression of myocardial nuclear factor kappa B (NF-kappaB), and the plasma content of NF-kappaB in rats with chronic heart failure.
Methods:
The chronic heart failure (CHF) model in rats was induced by coronary artery ligation. Sham operation was performed in control rats. Six weeks after the procedure, rats were randomly classified into the various treatment groups: model CHF, Captopril (4.4 mg/kg), low LGZGD dose (2.1 g/kg), medium LGZGD dose (4.2 g/kg), and high LGZGD dose (8.4 g/kg). Treatments continued for 4 consecutive weeks. Changes of hemodynamic indices were observed by the PowerLab data acquisition and analysis system. Morphological changes of myocardium were observed by hematoxylin and eosin staining, and Masson staining. The mRNA and protein expression of myocardial NF-kappaB were detected by reverse transcription-polymerase chain reaction and western blotting, respectively. The plasma content of NF-kappaB was detected by enzyme-linked immuno-sorbent assay.
Results:
CHF rats showed significant dysfunction in hemodynamic indices and in cardiac structure. Compared with the sham operation group, mRNA expression of myocardial NF-kappaB and plasma content of NF-kappaB of the model group was significantly increased. All three doses of LGZGD, and Captopril, improved the hemodynamic dysfunction, and inhibited the change of cardiac structure while significantly improving the survival rate. Furthermore, compared with the model group, mRNA expression of myocardial NF-kappaB and plasma content of NF-kappaB were significantly reduced by all dosage groups of LGZGD as well as the Captopril group.
Conclusion:
In CHF rats, LGZGD improves changes of cardiac structure and function via its inhibition of NF-kappaB.
