Apigenin, a flavonoid with multiple physiological and pharmacological activities, is associated with the prevention of cardiovascular diseases. The present study aimed to examine the roles and mechanisms of apigenin in the apoptosis of H9C2 rat cardiomyocytes, which were subjected to myocardial ischemia-reperfusion (MI/R) injury. Cell viability, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and cellular apoptosis were evaluated using cell counting kit-8 assays and flow cytometry. The content/activity of oxidative stress markers was determined using commercial kits. Western blot analysis and reverse transcription-quantitative polymerase chain reaction assays were used to measure protein and mRNA expression, respectively. The results demonstrated that apigenin had limited cytotoxicity on the viability of H9C2 rat cardiomyocytes. Apigenin reduced the oxidative stress, ROS production and cellular apoptotic capacity of MI/R-induced H9C2 cells. Apigenin additionally increased the MMP level of MI/R-induced H9C2 cells. Furthermore, apigenin modulated apoptosis-associated protein expression and phosphatidylinositol 3′-kinase (PI3K)/RAC-α serine/threonine-protein kinase (Akt) signaling in MI/R-induced H9C2 cells. Treatment with LY294002 reversed the anti-apoptotic effect of apigenin. In conclusion, apigenin suppressed the apoptosis of H9C2 cells that were subjected to MI/R injury by activating the PI3K/Akt pathway. It was suggested that apigenin may be effective as an MI/R therapy.

Background:Acori Tatarinowii Rhizoma (ATR), a traditional Chinese herbal medicine, is used to treat Alzheimer's disease (AD), which is a worldwide degenerative brain disease. The aim of this study was to identify the potential mechanism and molecular targets of ATR in AD by using network pharmacology. Material/Methods:The potential targets of the active ingredients of ATR were predicted by PharmMapper, and the targets of Alzheimer's disease were searched by DisGeNET. All screened genes were intersected to obtain potential targets for the active ingredients of ATR. The protein-protein interaction network of possible targets was established by STRING, GO Enrichment, and KEGG pathway enrichment analyses using the Annotation of DAVID database. Next, Cytoscape was used to build the "components-targets-pathways" networks. Additionally, a "disease-component-gene-pathways" network was constructed and verified by molecular docking methods. In addition, the active constituents b-asarone and b-caryophyllene were used to detect Ab 1-42 -mediated SH-SY5Y cells, and mRNA expression levels of APP, Tau, and core target genes were estimated by qRT-PCR. Results:The results showed that the active components of ATR participate in related biological processes such as cancer, inflammation, cellular metabolism, and metabolic pathways and are closely related to the 13 predictive targets: ESR1, PPARG, AR, CASP3, JAK2, MAPK14, MAP2K1, ABL1, PTPN1, NR3C1, MET, INSR, and PRKACA. The ATR active components of b-caryophyllene significantly reduced the mRNA expression levels of APP, TAU, ESR1, PTPN1, and JAK2. Conclusions:The targets and mechanism corresponding to the active ingredients of ATR were investigated systematically, and novel ideas and directions were provided to further study the mechanism of ATR in AD.

Podocytes are a special type of differentiated epithelial cells that maintain the glomerular filtration barrier in the kidney. Injury or damages in podocytes can cause kidney-related disorders, like CKD. The injury or dysfunction of podocytes can occur by different metabolic disorders. Due to the severity and complexity of podocyte injuries, this state is considered as a serious health issue worldwide. Here, we examined and addressed the efficacy of an alternative Chinese medicine, Shen Qi Wan (SQW), on podocyte-related kidney injury. We evaluated the role and mechanism of action of SQW in podocyte injury. We observed that SQW significantly reduced 24-hour urinary protein and blood urea nitrogen levels and alleviated the pathological damage caused by adenine. Moreover, SQW significantly decreased the expression of nephrin and increased the expression of WT1 and AQP1 in the kidney of mice treated with adenine. We observed that SQW did not effectively reduce the high level of proteinuria in AQP1−/− mice indicating the prominent role of AQP1 in the SQW-ameliorating pathway. Transmission electron microscopy (TEM) images indicated the food processes effacement in AQP1−/− mice were not lessened by SQW. In conclusion, podocyte injury could alter the pathological nature of the kidney, and SQW administration relieves the nature of pathogenesis by activating AQP1.

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