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. 2013 Jun;33(3):343-8.
doi: 10.1016/s0254-6272(13)60176-4.

Effect of lingguizhugan decoction on myocardial nuclear factor kappa B protein expression in rats with chronic heart failure

Jinling Huang  1 , Liang Wang, Hui Shi, Xiaoyan Hou
Affiliations
Free article

Effect of lingguizhugan decoction on myocardial nuclear factor kappa B protein expression in rats with chronic heart failure

Jinling Huang et al. J Tradit Chin Med. 2013 Jun.
Free article

Abstract

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.

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