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Updated: May 20, 2026

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
Published on: April 30, 2020
[Dynamic correlation of TNF-α and IL-10 with myocardial remodeling induced by pressure overload in rats]
Ju-rong Zeng1, Xiao-li Xu, Xiao-jiang Yu
1Department of Pharmacology, Xi'an Medical University, China. jrzeng988@hotmail.com
Aim:
To observe the expression changes of tumor necrosis factor alpha (TNF-α) and interleukin-10 (IL-10) during the developing process of pressure overload-induced myocardial remodeling in rats, and investigate the dynamic correlation between TNF-α and left ventricular mass index (LVMI) as well as myocardial collagen volume fraction (CVF).
Methods:
The rats (n=56) were randomly divided into control group, sham operation group and model group. Animal models were induced by abdominal aortic constriction (AAC). AAC group was further divided into 2 weeks, 4 weeks, 8 weeks and 12 weeks groups. Dynamic expression changes of TNF-α and IL-10 were tested by enzyme-linked immunosorbent assay(ELISA), and myocardial collagen fiber was observed by Mallory's staining.
Results:
Myocardial cells became increasingly disarranged, filaments broken, intercellular space increased, and collagen fiber accumulated 4 weeks after operation. Furthermore, heart failure occurred 12 weeks after operation. ABC-ELISA results showed that TNF-α expression in myocardium increased at 4, 8, 12-week operation groups in a time-dependent fashion compared with control group (P<0.01); Correlation analysis indicated the expression of TNF-α in myocardium was positively correlated with LVMI (r=0.582, P<0.01) and CVF (r=0.932, P<0.01); IL-10 expression in myocardium among groups were similar, but the ratio of TNF-α and IL-10 increased in a time-dependent manner, from (1.79 ± 0.19) ng/mL (2 weeks) up to (2.85 ± 0.24) ng/mL(12 weeks) as compared with control group (1.74 ± 0.24) ng/mL (P<0.01).
Conclusion:
The degree of myocardial remodeling plays a key role in heart function deterioration, and the TNF-α expression up-regulation in a time-dependent manner and the disproportion of TNF-α and IL-10 is one of important molecular mechanisms.
