The Effects of 17-Methoxyl-7-Hydroxy-Benzene-Furanchalcone on Pressure Overload-Induced Cardiac Remodeling in Rats and the Endothelial Mechanisms Based on PGI2

Abstract

Aim: The primary objective of this study was to study the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC) on pressure overload-induced cardiac remodeling in rats, as well as the endothelial mechanisms based on PGI₂. Methods: Six weeks following surgery, rats were divided randomly into the following groups: a sham group, a model group, an MHBFC 12 mg/kg/day group (MHBFC 12), an indomethacin 2 mg/kg/day group (Indo 2), and an Indo 2+ MHBFC 12 group. The MS 4000 organism signal system was used to record the rats' hemodynamic indices. Additionally, the heart weight was determined, and the cardiac remodeling index was calculated. HE and Masson's stains were utilized to perform histological analyses; the immunofluorescence was used to observe the microvessel density of myocardial tissue; the colorimetric method was used to determine the hydroxyproline content of cardiac tissue; the ELISA method was used to measure the plasma PGI₂ content; and transmission electron microscopy was used to observe the ultrastructure of the myocardium. Results: A hyperdynamic circulation state, cardiac remodeling, decreased microvessel density and decreased plasma PGI₂ content were each observed in the model group compared with the sham group, in which any changes in the above parameters were effectively reversed by MHBFC. Single-use Indo administration resulted in the progression of these pathophysiological changes; however, MHBFC prevented the worsening of these parameters. Conclusion: MHBFC significantly reverses pressure overload-induced cardiac remodeling, and its mechanism may partially contribute to the amelioration of endothelial cell function and the augmentation of PGI₂ synthesis and secretion.

Contributions of Nrf2 to Puerarin Prevention of Cardiac Hypertrophy and its Metabolic Enzymes Expression in Rats

“…The rats were housed in an environmentally controlled room (temperature, 25 6 2°C; humidity, 60% 6 5%; 12-hour dark/light cycle) with access to regular chow diet ad libitum for 1 week before the experiments. Cardiac hypertrophy was induced by abdominal aortic constriction (AAC), which was modified based on a previously reported procedure (Reddy et al, 1996;Huang et al, 2015;Ku et al, 2016). In brief, the rats were anesthetized using pentobarbital (45 mg/kg, i.p.…”

The Vasodilator Effect and Mechanism of 18β-glycyrrhetinic Acid on Isolated Pulmonary Artery Rings in Rats

“…PGI2 is regarded as having a preventive impact in vascular disorders as it is a potent vasodilator of vascular smooth muscle that can decrease platelet aggregation. In the body, PGI2 acts on the corresponding IP receptors by activating adenylate cyclase and increasing the content of cAMP, which causes a vasodilation response (Huang et al, 2015; Liu & Zhou, 2021; Sugita et al, 2016). INDO is a Cyclooxygenase (Cox) inhibitor.…”