Experimental research on the evaluation of left ventricular systolic function by layered speckle tracking before and after berberine treatment in a cardiac hypertrophy rat model.

ABSTRACT

Background: To evaluate the effect of berberine (BBR) intervention on left ventricular hypertrophy and systolic function in rats by ultrasound layered strain imaging and cardiac hypertrophy model. Methods: Eighty healthy male Sprague-Dawley (SD) rats were randomly divided into four groups group A (normal saline control group), group B [isoproterenol (ISO) induced model group], group C (BBR hydrochloride 5 mg/kg + ISO group) and group D (BBR hydrochloride 10 mg/kg + ISO group). Echocardiography was performed on days 1, 7 and 14, respectively. The myocardial tissue was taken for pathological examination. The key proteins of Rho/ROCK signaling pathway were quantified by immunohistochemical staining. Results: On day 7, compared with group A, peripheral strain values of the subendocardium and middle myocardium of rats in groups B, C and D were significantly decreased. The absolute value of circumferential strain (CS) in subendocardium and middle myocardium in group B was significantly lower than that in groups C and D (-24.21 vs. -26.68 vs. -27.69; -14.90 vs. -16.48 vs. -17.69). Pathological results showed that compared with the myocardial cells in control group A, the myocardial cells in group B had significantly increased cross-sectional area, and obvious myocardial interstitial fibrosis. Compared with group B, BBR intervention reduced the deposition of fibrosis in groups C and D, group D was more obvious. Immunohistochemical results showed that compared with group A, the protein expression levels of ROCK, RhoA and Bax in groups B, C and D were significantly increased, while the protein expression levels of Bcl-2 were significantly decreased. Conclusions: Ultrasound layered strain imaging could evaluate the early left ventricular systolic function in isoprenaline-induced hypertrophy rat model. BBR might inhibit oxidative stress through the Rho/ROCK signaling pathway and slow down the progression of myocardial fibrosis after the formation of cardiac hypertrophy. This provides reference and direction for clinical decision-making and further research.