Study on the effects and mechanisms of different oils on spatial learning and memory in developing rats. Fifty-six Sprague Dawley (SD) rats with primary weaning were randomly divided into the 7 groups, DHA, walnut oil, perilla oil, safflower seed oil, α-linoleic acid, and Essential fatty acid (EFA)-deficient and negative control. Morris water maze behavioral test was performed after 8 weeks of continuous feeding. Real-time fluorescence quantification and immunoblotting were performed to evaluate changes in the expression of NR1, CREB and c-Fos in rat hippocampus, qPCR detected the expression in hippocampal cells. The results showed that the rats fed various oils significant improvement in the Morris water maze test. The mRNA expression of NR1, CREB and c-Fos in the hippocampus of rats fed with various oils were significantly up-regulated (P<0.05 and P<0.01), and CREB and c-Fos proteins expression were up-regulated (P<0.05). The expression of genes and proteins in hippocampus of EFA-deficient control was not significantly different from negative control. It is suggested that polyunsaturated fatty acids could significantly improve the learning and memory ability of rats, which may be through regulating the mRNA expression of cfos, CREB and NR1 in rat hippocampus and the synthesis of CREB and c-Fos proteins.

Background: 1,2,3,4,6-Penta-O-galloyl-β-D-glucose (β-PGG) is a polyphenol ellagic compound with a variety of pharmacological effects and has an inhibitory effect on lots of cancers. Objective: To explore the antitumor effects and mechanism of 1,2,3,4,6-Penta-O-galloyl-β-D-glucose on human hepatocellular carcinoma HepG2 cells. Design: A network pharmacology method was first used to predict the possible inhibition of hepatocellular carcinoma growth by 1,2,3,4,6-Penta-O-galloyl-β-D-glucose (β-PGG) through the p53 signaling pathway. Next, the Cell Counting Kit (CCK-8) assay was performed to evaluate changes in the survival rate of human hepatocellular carcinoma HepG2 cells treated with different concentrations of the drug; flow cytometry was used to detect changes in cell cycle, apoptosis, mitochondrial membrane potential (MMP) and intracellular Ca2+ concentration; real-time fluorescence quantification and immunoblotting showed that the expression of P53 genes and proteins associated with the p53 signaling pathway was significantly increased by β-PGG treatment. Reasult: It was found that β-PGG significantly inhibited survival of HepG2 cells, promoted apoptosis, decreased MMP and intracellular Ca2+ concentration, upregulated P53 gene and protein expression, increased CASP3 expression, and induced apoptosis in HepG2 cells. Conclusion: This study has shown that network pharmacology can accurately predict the target of β-PGG’s anti-hepatocellular carcinoma action. Moreover, it was evident that β-PGG can induce apoptosis in HepG2 cells by activating the p53 signaling pathway to achieve its anti-hepatocellular carcinoma effect in vitro.

The main aim of this study was to explore the antitumor effects and mechanism of 1,2,3,4,6-Penta-O-galloyl-β-D-glucose on human hepatocellular carcinoma HepG2 cells. A network pharmacology method was first used to predict the possible inhibition of hepatocellular carcinoma growth by β-PGG through the p53 signaling pathway. Next, the CCK-8 assay was performed to evaluate changes in the survival rate of human hepatocellular carcinoma HepG2 cells treated with different concentrations of the drug; flow cytometry was used to detect changes in cell cycle, apoptosis, mitochondrial membrane potential, and intracellular Ca2+ concentration; and real-time fluorescence quantification and immunoblotting were performed to evaluate changes in the expression of P53, BAX, and BCL-2. Results showed that the expression of P53 genes and proteins associated with the p53 signaling pathway was significantly increased by β-PGG treatment. It was found that β-PGG significantly inhibited survival of HepG2 cells, promoted apoptosis, decreased mitochondrial membrane potential and intracellular Ca2+ concentration, upregulated P53 gene and protein expression, increased CASP3 expression, and induced apoptosis in HepG2 cells. In conclusion, this study has shown that network pharmacology can accurately predict the target of β-PGG's anti-hepatocellular carcinoma action. Moreover, it was evident that β-PGG can induce apoptosis in HepG2 cells by activating the p53 signaling pathway to achieve its anti-hepatocellular carcinoma effect in vitro.

Corilagin has several pharmacological effects such as anti-tumor, anti-inflammatory, and cardiovascular disease treatment. Our previous studies have shown that the Corilagin can significantly inhibit proliferation of HeLa cells. However, there is no scientific data on the anti-cervical cancer effect of Corilagin in vivo. It was speculated that the mechanism of action for the anti-cervical cancer of Corilagin could be related to PI3K/AKT and MAPK signaling pathways through network pharmacology. Results of cell assays in the present study showed that the Corilagin has significant effect on the proliferation, cell cycle and apoptosis of murine cervical cancer U14 cells in vitro. In addition, Corilagin can significantly inhibit the growth of U14 tumor-bearing mice with insignificant toxic effect on liver and kidney of the transplanted mice. The current study found that Corilagin can delay development of cervical cancer by boosting anti-tumor immune responses of body. RT-PCR and Western blotting were applied in the current study to evident that Corilagin can achieve anti-cervical cancer property by inducing apoptosis of tumor tissues through both PI3K/AKT and MAPK signaling pathways. Therefore, this study provided theoretical reference for research of Corilagin as a bio-resource for development of an anti-cervical cancer drug and functional food.

The main aim of this study was to explore the antitumor effects and mechanism of 1,2,3,4,6-Penta-O-galloyl-β-D-glucose on human hepatocellular carcinoma HepG2 cells. A network pharmacology method was first used to predict the possible inhibition of hepatocellular carcinoma growth by β-PGG through the p53 signaling pathway. Next, the CCK-8 assay was performed to evaluate changes in the survival rate of human hepatocellular carcinoma HepG2 cells treated with different concentrations of the drug; flow cytometry was used to detect changes in cell cycle, apoptosis, mitochondrial membrane potential, and intracellular Ca2+ concentration; and real-time fluorescence quantification and immunoblotting were performed to evaluate changes in the expression of P53, BAX, and BCL-2. Results showed that the expression of P53 genes and proteins associated with the p53 signaling pathway was significantly increased by β-PGG treatment. It was found that β-PGG significantly inhibited survival of HepG2 cells, promoted apoptosis, decreased mitochondrial membrane potential and intracellular Ca2+ concentration, upregulated P53 gene and protein expression, increased CASP3 expression, and induced apoptosis in HepG2 cells. In conclusion, this study has shown that network pharmacology can accurately predict the target of β-PGG's anti-hepatocellular carcinoma action. Moreover, it was evident that β-PGG can induce apoptosis in HepG2 cells by activating the p53 signaling pathway to achieve its anti-hepatocellular carcinoma effect in vitro.