Protective Effect of Naringenin on Acute Myocardial Ischemia-reper-fusion Injury in Rats.

Xia ZHANG; Ping ZHOU; Juan LI; Zhaojun XIANG; Qianqian LUO; Qing DENG

[Objectives] To investigate the protective mechanism of naringenin on acute myocardial ischemia-reperfusion injury (AMI-RI) in Sprague-Dawley (SD) rats. [Methods] A total of 32 SD rats with AMI-RI model construction were randomly divided into AMI-RI model control group and citrus pigment A/B/C groups (n = 8). The naringenin A, B, and C groups were administrated 20, 40 and 80 mg/(kg - d) for 10 d. The AMI group served as the negative control and was not treated. At the conclusion of the treatment regimen, a sample of intraventricular blood was collected for the purpose of measuring lactate dehydrogenase (LDH), glutathione peroxidase (GLH-PX), nitric oxide (NO), and superoxide dismutase (SOD) levels. Additionally, myocardial tissue was identified within the ischemic region. The content of malondialdehyde (MDA) was determined by inducing nitric oxide synthase (iNOS) and endodermal nitric oxide synthase (eNOS) positive cells in the left anterior descending coronary artery. [Results] Following citrus treatment, the contents of GLH-PX and SOD in ventricular blood of the citrus B group were found to be significantly elevated, while the contents of NO and LDH in myocardial MDA and ventricle were observed to be significantly reduced. The number of eNOS-positive cells was significantly increased, while the number of iNOS-positive cells was significantly decreased. The difference was statistically significant when compared with the AMI-RI group (P <0.05). The changes observed in the above indicators in the citrus C group were more pronounced than those observed in the citrus B group. The difference between the citrus C and the B group was statistically significant (P <0.05), indicating that this effect is concentration dependent. [Conclusions] In addition to its ability to inhibit myocardial lipid peroxidation during AMI-RI by increasing SOD activity, naringenin may also affect the synthesis and release of NO by regulating eNOS and iNOS, thereby achieving protection against AMI-RI. One effect is enhanced as the dose of the drug increases.

NITRIC-oxide synthases; LABORATORY rats; LACTATE dehydrogenase; SUPEROXIDE dismutase; GLUTATHIONE peroxidase

Medicinal Plant, 2024, Vol 15, Issue 3, p50

2152-3924

Academic Journal

10.19600/j.cnki.issn2152-3924.2024.03.012