Anshen Buxin Liuwei Pill, a Mongolian Medicinal Formula, Could Protect H2O2-Induced H9c2 Myocardial Cell Injury by Suppressing Apoptosis, Calcium Channel Activation, and Oxidative Stress

Abstract

Background. Anshen Buxin Liuwei pill (ABLP) is a Mongolian medicinal formula which has a therapeutic effect on the symptoms such as coronary heart disease, angina pectoris, arrhythmia, depression and irritability, palpitation, and short breath. However, its bioactivity against cardiac injury remains unclear. Methods. The protective effect of ABLP was evaluated using H9c2 cells. Cell viability, intracellular Ca2+, reactive oxidative indices, and mitochondrial membrane potential (∆ψ) were assessed, respectively. The mRNA levels of Ca2+ channel-related genes (DHPR, RyR2, and SCN5A) and oxidative stress-related genes (Keap1, Nrf2, and HO-1) were measured by RT-PCR. Results. 0.5–50 μg/mL ABLP could significantly decrease H2O2-induced cell injury by suppressing cell necrosis/apoptosis and excess oxidative stress, ameliorating the collapse of ∆ψ, and reducing intracellular Ca2+ concentration. Furthermore, 0.5–50 μg/mL ABLP reversed H2O2-induced imbalance in the mRNA levels of DHPR, RyR2, SCN5A, Keap1, Nrf2, and HO-1 gene in H9c2 cells, which further illustrate the mechanism. Conclusion. ABLP provided protective and therapeutic benefits against H2O2-induced H9c2 cell injury, indicating that this formula can effectively treat coronary disease. In addition, the present study also provides an in-depth understanding of the pharmacological functions of ABLP, which may lead to further successful applications of Mongolian medicine.

N-Acetylcysteine, an ROS Inhibitor, Alleviates the Pathophysiology of Hyperthyroidism-Induced Cardiomyopathy via the ROS/Ca2+ Pathway

“…Combining these results, the animal and cell model simulated the process of heart disease caused by hyperthyroidism, which could be applied to investigate the molecular mechanism. As shown in Figure 11 , an increase in Cav1.3 induces an increase in the cytosolic Ca 2+ concentration of H9c2 cells, thereby increasing the activation of Ca 2+ -dependent signalling, Rcan1, calcineurin, and calpain, which subsequently upregulates the gene expression of hypertrophy markers and upregulates the gene expression of inflammatory cytokines by activating the NF-κB/p65-dependent signalling pathway [ 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 ], causing cardiac hypertrophy and inflammation. Meanwhile, the elevation of Gal-3, RhoA, and Rock further increased ROS [ 27 , 28 , 29 , 30 , 31 , 32 ], subsequently regulating the Bcl-2/caspase-3-dependent apoptotic signalling pathway [ 33 , 34 ], thereby leading to cell rupture and fibrosis.…”

Network Pharmacology-Based Combined with Experimental Validation Study to Explore the Underlying Mechanism of Agrimonia pilosa Ledeb. Extract in Treating Acute Myocardial Infarction

“…[10][11][12][13] Oxidative stress can induce both oxidative damage and apoptosis, and moderate apoptosis can protect cardiomyocytes from damage in stressful conditions. [14][15][16] Excessive oxidative stress can promote apoptosis and even lead to pathological damage. 17 The phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway is a significant intracellular signal transduction route that has a protective function in apoptosis.…”