Ginsenoside Rb3 (GRb3) is an active ingredient extracted from Panax ginseng, which is known to enhance blood supply to heart and treat a variety of cardiac diseases. The aim of this study was to investigate the effect of GRb3 on myocardial injury induced by sleep deprivation and its mechanisms. GRb3 20 mg/kg group showed lower heart rate (438.2 ± 10.06 bpm), Creatine kinase (27.43 ± 2.85 U / mg prot) and Lactate dehydrogenase (412.9 ± 35.65 U / L) than SD group (592.0 ± 7.78 bpm, 44.18 ± 1.24 U / mg prot, 526.6 ± 38.18 U / L). GRb3 improved myocardial tissue damage and abnormal mitochondrial morphological changes. GRb3 also reduced the abnormal proteins expression of Atrial Natriuretic Peptide (ANP), Sirtuin3 (SIRT3), Tumor Protein P53 (P53), Solute Carrier Family 7 (SLC7A11), Glutathione peroxidase 4 (GPX4), Transferrin Receptor Protein 1 (TFRC), Acyl-CoA synthetase long chain family member 4 (ACSL4), Heme Oxygenase-1 (HO-1), Ferritin heavy polypeptide 1 (FTH1), Ferroptosis suppressor protein 1 (FSP1). GRb3 ameliorated oxidative stress, such as Malondialdehyde (MDA,), Glutathione (GSH), and Superoxide dismutase (SOD). GRb3 also decreased Reactive Oxygen Species (ROS) content, restored cellular abnormal mitochondrial morphology and reversed the expression of ferroptosis-related proteins on H9c2 cells pretreated with Erastin. While the above effect could be reversed by 3-TYP. In summary, GRb3 exerts cardioprotective effects by regulating SIRT3/P53/SCL7A11/GPX4 axis to inhibit myocardial ferroptosis in sleep deprived mice. The findings imply that GRb3 holds promising potential for innovative approaches to safeguarding human cardiac health.

Parkinson’s disease (PD) is a common neurodegenerative disorder with no cure. Astragalus membranaceus is used in Chinese culture as a food supplement to boost immunity. The present study aimed to explore the neuroprotective effects of total flavonoids extracted from A. membranaceus (TFA) and their protective mechanisms. TFA offered neuroprotection against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse model of Parkinsonism, by improving behavior performance in the gait analysis and pole test, and inhibiting the decline of tyrosine hydroxylase (TH) positive neurons and TH protein expression in substantia nigra of mice. TFA also prevented 1-methyl-4-phenylpyridinium (MPP⁺) induced neurotoxicity in SH-SY5Y cells, by increasing GSH and GSH/GSSG ratio, and reducing reactive oxygen species. In addition, the neuroprotective effects of TFA were associated with its ability to restore MPTP/MPP⁺ induced downregulation of SLC7A11 and glutathione peroxidase 4 (GPX-4). In conclusion, we demonstrated that TFA exerted significant neuroprotection against MPTP/MPP⁺ induced neurodegeneration by inhibiting ferroptosis through the regulation of SLC7A11/GPX-4 axis, suggesting the use of TFA as a possible food supplement in the prevention of PD.