Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Abstract

Liquiritigenin (Lq) offers cytoprotective effects against various cardiac injuries, but its beneficial effects on myocardial ischemic (MI) injury and the related mechanisms remain unclear. In the in vivo study, an animal model of MI was induced by intraperitoneal injection of isoproterenol (Iso, 85 mg/kg). ECG, heart rate, serum levels of CK and CK‐MB, histopathological changes, and reactive oxygen species (ROS) levels were all measured. In vitro, H9c2 cells were divided into four groups and treated for 24 hr with liquiritigenin (30 μmol/L and 100 μmol/L) followed with CoCl2 (800 μmol/L) for another 24 hr. Cell viability, apoptosis, mitochondrial membrane potential, and intracellular Ca2+ concentration ([Ca2+]i) were then assessed. The L‐type Ca2+ current (ICa‐L) was detected using a patch clamp technique on isolated rat ventricular myocytes. The myocyte contraction and Ca2+ transients were measured using an IonOptix detection system. The remarkable cardiac injury and generation of intracellular ROS induced by Iso were alleviated via treatment with Lq. CoCl2 administration induced cell apoptosis, mitochondrial dysfunction, and Ca2+ overload in H9c2; Lq reduces these deleterious effects of CoCl2. Meanwhile, Lq blocked ICa‐L in a dose‐dependent manner. The half‐maximal inhibitory concentration of Lq was 110.87 μmol/L. Lq reversibly reduced the amplitude of cell contraction as well as the Ca2+ transients. The results show that Lq protects against MI injury by antioxidation, antiapoptosis, counteraction mitochondrial dysfunction, and inhibition of ICa‐L, thus damping intracellular Ca2+.

Metabolite Profiling Analysis of the Tongmai Sini Decoction in Rats after Oral Administration through UHPLC-Q-Exactive-MS/MS

“…Metabolites of licorice flavonoids and 6-gingerol were also mainly detected. Liquiritigenin offers cytoprotective effects against various cardiac injuries, and it could protect against myocardial ischemic injury by antioxidation, antiapoptosis, counteraction mitochondrial dysfunction, and damping intracellular Ca 2+ [ 43 ]. 6-Gingerol was identified as a novel angiotensin II type 1 receptor antagonist for cardiovascular disease by high-throughput screening, which partially clarified the mechanism of ginger regulating blood pressure and strengthening the heart [ 44 ].…”

Interpreting the Mechanism of Active Ingredients in Polygonati Rhizoma in Treating Depression by Combining Systemic Pharmacology and In Vitro Experiments

“…DFV is a flavonoid compound widely present in Chinese herbal medicines such as PR, Glycyrrhizae radix et rhizome (Pharmacopoeia of China, 2015), Isatidis folium (Pharmacopoeia of China, 2015), Hedysari Radix (Pharmacopoeia of China, 2015), Epimedii folium (Pharmacopoeia of China, 2015), etc. The liver- and heart-protective effects of DFV have been extensively studied [ 26 , 73 , 74 , 75 ]. In addition, there have been some reports on the neuroprotective effects of DFV that we are concerned about.…”

“…DFV belongs to the flavonoid compounds in PR. Previous studies have shown that DFV has liver protection [ 25 ], anti-myocardial ischemia [ 26 ], anti-breast cancer [ 27 ], and bone protection effects [ 28 , 29 ]. In these studies, DFV demonstrated strong anti-inflammatory and antioxidant stress-resistance abilities.…”

Shenxiong glucose injection inhibits oxidative stress and apoptosis to ameliorate isoproterenol-induced myocardial ischemia in rats and improve the function of HUVECs exposed to CoCl2

“…As a clinically marketed drug, SGI has shown curative effects in clinical experiments ( Sun et al, 2017 ). Oxidative damage is an important pathophysiological basis for the occurrence and development of MI ( Zhang M. et al, 2022 ). In this study, we found that the effects of SGI against MI occur through inhibitin of oxidative stress and apoptosis pathways.…”