Leonurine has been shown to have excellent anti-myocardial ischemia effects. Our previous studies suggested that cardiac protection by leonurine during myocardial ischemia appeared to be inextricably linked to its regulation of the liver. At present, however, there are few mechanistic studies of leonurine and its regulation of hepatic metabolism against ischemic injury. In this study, a metabolomics approach was developed to give a global view of the metabolic profiles of the heart and liver during myocardial ischemia. Principal component analysis and orthogonal partial least squares discrimination analysis were applied to filter differential metabolites, and a debiased sparse partial correlation analysis was used to analyze the correlation of the differential metabolites between heart and liver. As a result, a total of thirty-one differential metabolites were identified, six in the myocardial tissue and twenty-five in the hepatic tissue, involving multiple metabolic pathways including glycine, serine and threonine, purine, fatty acid, and amino acid metabolic pathways. Correlation analysis revealed a net of these differential metabolites, suggesting an interaction between hepatic and myocardial metabolism. These results suggest that leonurine may reduce myocardial injury during myocardial ischemia by regulating the metabolism of glycine, serine and threonine, purine, fatty acids, and amino acids in the liver and heart.

Alzheimer’s disease (AD), characterized by progressive cognitive decline and functional impairment, is the most prevalent cause of dementia, and it poses a significant socioeconomic and caregiving burden on patients, families, and healthcare systems. Notwithstanding comprehensive research, the precise causes underlying AD remain ambiguous. Evidence increasingly indicates that AD is a multifactorial and heterogeneous disease involving a mix of genetic and environmental factors. The amyloid-cascade hypothesis, neuroinflammation and immunity, vascular pathology, and oxidative stress all fulfill significant functions in the onset and development of AD. This review primarily examines the critical pathogenesis, key biomarkers, and novel therapeutic strategies of Alzheimer’s disease to inform future research directions.

Oxypeucedanin, a furanocoumarin extracted from many traditional Chinese herbal medicines, has a variety of pharmacological effects. However, the independent pharmacokinetic characteristics and bioavailability of this compound remains elusive. In this study, a rapid, sensitive, and selective method using ultra-high performance liquid chromatography–tandem mass spectrometry (UPLC/MS/MS) was developed for evaluating the intravenous and oral pharmacokinetics of oxypeucedanin. After intravenous administration of oxypeucedanin (2.5, 5, and 10 mg/kg), and intragastric administration of oxypeucedanin (20 mg/kg), blood samples were collected periodically from the tail vein. The plasma concentration-time curves were plotted, and the pharmacokinetic parameters were calculated using a non-compartmental model analysis. After intravenous administration of oxypeucedanin (single dosing at 2.5, 5, and 10 mg/kg) to rats, the pharmacokinetics fit the linear kinetics characteristics, which showed that some parameters including average elimination half-life (T_1/2Z of 0.61~0.66 h), mean residence time (MRT of 0.62~0.80 h), apparent volume of distribution (V_Z of 4.98~7.50 L/kg), and systemic clearance (CL_Z of 5.64~8.55 L/kg/h) are dose-independent and the area under concentration-time curve (AUC) increased in a dose-proportional manner. Single oral administration of oxypeucedanin (20 mg/kg) showed poor and slow absorption with the mean time to reach the peak concentration (T_max) of 3.38 h, MRT of 5.86 h, T_1/2Z of 2.94 h, and a mean absolute bioavailability of 10.26% in rats. These results provide critical information for a better understanding of the pharmacological effect of oxypeucedanin, which will facilitate its research and development.