Search

Background Diabetic nephropathy (DN), a unique complication of diabetes, could contribute to an increase in mortality. In this study, we predicted and proved the molecular pharmacological mechanism concerning the protective effects of Astragali Radix on DN. Methods The same potential target genes from Astragali Radix and DN were analyzed and constructed the protein interaction network. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment-related major targets and signal pathways were performed. The drug-ingredients-target-disease network was visually built using Cytoscape 3.6.1. The beneficial pharmacological activities of quercetin from Astragali Radix were confirmed by CCK-8 assay, determination of antioxidant parameters and Western blotting analysis. Results There are 12 bioactive components from Astragali Radix and 56 same targets between Astragali Radix and DN. The GO analysis results showed that the biological processes mainly included protein homodimerization activity. KEGG analysis indicate that the screened targets were most closely linked to the mitogen-activated protein kinase (MAPK) signaling pathway. The drug-ingredients-target-disease network results revealed that the therapeutic effects of Astragali Radix mainly included oxidative stress, inflammatory reaction and apoptosis. During the verification process, quercetin from Astragali Radix could attenuate cytotoxicity, enhance catalase (CAT) and superoxide dismutase (SOD) activities and suppress MAPK signaling pathway. Conclusions In the current study, network pharmacology with experimental analysis predicted and proved the therapeutic function of Astragali Radix by improving antioxidant capacity and suppressing MAPK signaling pathway, these investigations could provide a new perspective for further exploration of Astragali Radix on DN treatment.

To investigate the anti-obesity and hypolipidemic effects of Alpinia officinarum ethanolic extract (AOE) for the first time, anti-obesity models in vivo were used. Ten male Sprague-Dawley rats were fed normal control diet (NC); other groups of rats were fed a high-fat diet (HFD) with or without different proportions of AOE (AOE-1, 3%; AOE-2, 5%) for 6 weeks to examine feed intake, body and adipose tissue weight, serum total cholesterol (Total-C), triacylglycerol (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and leptin levels, alanine aminotransferase (ALT) and aspartate aminotranferase activities, hepatic Total-C and TG levels, and the pathological changes in liver and epididymal adipose tissues. Interestingly, feed intakes among the experimental groups were not significantly different. Body weight gains were significantly lowered in the AOE-1 and AOE-2 groups compared with the HFD group (P < .05) and near to the level of the NC group. AOE also improved the lipid profile in serum and the pathological changes in liver and adipose tissue and decreased the relative weights of epididymal and perirenal white adipose tissues. They improved lipid profile by lowering serum Total-C, TG, and LDL-C concentrations, leptin content, and the atherogenic index compared with the HFD group. The HDL-C concentration and the ratio of HDL-C/Total-C significantly increased compared with those of the HFD group. The serum ALT activity of the AOE-2 group was notably lower than that of the HFD group. Our data suggest that AOE can be considered as an anti-obesity agent that is effective for suppressing body weight gain and decreasing lipid profile.

The protective effects of puerarin on liver damage were evaluated by carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. Male rats were orally treated with puerarin daily, and received CCl4 intraperitoneally twice a week for 4 weeks. Our results showed that puerarin at doses of 50, 100, and 200 mg/kg b.w. significantly reduced the elevated activities of serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase at least 15%, 17%, 14% and 18%, respectively. In addition, puerarin at different doses significantly decreased (p < 0.05) the level of hepatic thiobarbituric acid reactive substances compared to the CCl4-treated group. Furthermore, the treatment of puerarin was also found to significantly increase the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and glutathione content at least 40%, 12%, 25%, 52%, 17% and 44% in the liver of CCl4-treated rats, respectively. Liver histopathology also showed that puerarin reduced the incidence of liver lesions induced by CCl4. The results suggest that puerarin exhibits potent hepatoprotective effects on CCl4-induced liver damages in rats, and that the hepatoprotective effects of puerarin may be due to both the inhibition of lipid peroxidation and to increase of antioxidant enzymes activity.