Qi-Ge decoction (QGD), which is derived from the Huangqi Gegen decoction, contains three traditional Chinese herbs: Astragalus membranaceus (Huangqi), Pueraria lobata (Gegen), and Citri Reticulatae Blanco Pericarpium (Chenpi). Gastric mucosal damage caused by ethanol was prevented and alleviated by QGD. However, the role of QGD in protecting the liver from toxins has not been reported. High-performance liquid chromatography with diode-array detection was used to qualitatively analyze QGD. Positive control (silymarin 100 mg/kg/day), QGD (20, 10, or 5 g/kg/day), and Nrf2 inhibitor brusatol (0.4 mg/kg/2 d) were administered to rats for 7 days, and then, liver injury was induced by injecting 2 mL/kg 25% CCl4. After 24 h, blood and liver were collected for analysis and evaluation. QGD was found to contain 12 main components including calycosin, puerarin, and hesperidin. QGD treatment significantly reduced liver damage and decreased serum alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase activities. QGD increased superoxide dismutase and catalase activities, and glutathione levels, but decreased malondialdehyde levels in livers from CCl4-treated rats. Compared to rats treated with CCl4 alone, after QGD administration, mRNA and protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 were increased, while those of Kelch-like ECH-related protein 1 (Keap1) and cytochrome P450 (CYP)2E1 were decreased. However, these improvements in QGD were reversed by brusatol. In conclusion, QGD can achieve its hepatoprotective effect through an antioxidant mechanism by activating the Nrf2 pathway.

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Manual acupuncture (MA) can be used to manage high blood pressure; however, the underlying molecular mechanism remains unknown. To explore the mechanism of acupuncture in the treatment of hypertension, Wistar Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) were subjected to either MA stimulation or the corresponding sham procedure as a negative control (Sham-MA) for 1 week. PET-CT scans, transcriptomics and molecular biology were used to evaluate the effect of MA. The results show that MA can regulate blood pressure in SHRs, change the glucose metabolism of the paraventricular hypothalamus (PVH), and affect the mRNA and protein expression levels of differentially expressed genes in the PVH. These genes may lower blood pressure by regulating angiotensin, endothelial function and inflammation. These findings reveal that MA regulates multiple biological processes and genes/proteins of the PVH, and provide a solid theoretical basis for exploring the mechanisms by which MA regulates hypertension.

The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing as obesity and diabetes become more common. There are no drugs approved for NAFLD yet. Qige decoction (QGD), a traditional Chinese medicine (TCM) formula, is used for NAFLD and hyperlipidemia treatment in TCM and has shown hypolipidemic and hepatoprotective effects. This study tried to interpret the pharmacology and molecular mechanisms of QGD in NAFLD rats. Firstly, the therapeutic effects of QGD on high-fat diet (HFD)-induced NAFLD rats were evaluated. Then, integration of lipidomics and transcriptomics was conducted to explore the possible pathways and targets of QGD against NAFLD. QGD at low dosage (QGL) administration reduced serum total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) ( P < 0.05 ). Liver histopathology indicated that QGL could alleviate hepatic steatosis. The main differential lipids (DELs) affected by QGD were glycerolipids. KEGG enrichment analysis suggested that the main pathways by which QGD improved NAFLD may be cholesterol metabolism, glycerolipid metabolism, and insulin resistance. Transcriptome sequencing identified 179 upregulated and 194 downregulated mRNAs after QGD treatment. An interaction network based on DELs and differential genes (DEGs) suggested that QGD inhibited hepatic steatosis mainly by reducing hepatic insulin resistance and triglyceride biosynthesis via the PPP1R3C/SIK1/CRTC2 and PPP1R3C/SIK1/SREBP1 signal axis, respectively. These findings indicated that QGD could protect against NAFLD induced by HFD. The improvement of hepatic insulin resistance and the reduction of triglyceride biosynthesis might be the potential mechanisms.