Xing-Qi-Tong-Qiao Decoction (XQTQ) is a traditional Chinese prescription that embodies the homology of medicine and food. It is recognized for its effects in alleviating stasis, dispersing phlegm and nodules, activating blood circulation, relieving pain. However, its efficacy and mechanisms in alleviating paclitaxel-induced peripheral neuropathic pain (PIPNP) remain unclear. In this study, we investigate the analgesic effects of XQTQ and explore the potential mechanism using plasma metabolomics. The characteristic chromatogram of XQTQ was established using HPLC. A total of 36 SD rats were divided into 6 groups: control, model, positive drug, and three XQTQ combined groups. All rats, except those in control group, were induced with diseases features via intraperitoneal administration of paclitaxel. The pregabalin and XQTQ combined groups were administered orally once a day for 14 days. The paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were measured. Rat plasma was collected for the detection of pain cytokines and the analysis of endogenous metabolite. Rats in the XQTQ combined groups exhibited a significant increase in PWT and PWL values, alongside a decrease in the levels of tumor necrosis factor-alpha (TNF-α, 14.82%), interleukin-6 (IL-6, 13.69%), interleukin-1 beta (IL-1β, 19.34%), nerve growth factor (NGF, 11.40%), prostaglandin E2 (PGE 2, 12.74%), and 5-hydroxytryptamine (5-HT, 13.51%) compared to the model group (P < 0.01). Plasma metabolomics revealed 12 potential biomarkers associated with the model rats, which were significantly reversed by XQTQ. The main pathways involved included glycerophospholipid metabolism, linoleic acid (LA) metabolism, and alpha-linolenic acid (ALA) metabolism. XQTQ demonstrated significant analgesic effects and improved metabolism in the context of PIPNP. This research provides a reliable theoretical basis and novel research directions for clinical applications.

Obesity is a metabolic disorder due to over-accumulation of adipose tissue and ultimately becomes a “disease”. Brown adipose tissue (BAT) thermogenesis and white adipose tissue (WAT) browning emerge as a potential strategy of anti-obesity by dissipating energy as heat. However, drugs based on adipose tissue thermogenesis have not been successfully approved yet. In current study, we found that black tea extract (BTE) obtained by patent-authorized manufacturing process prevented body weight gain as novel thermogenic activator with reduction of adiposity, improvement of adipose distribution, and glucose metabolism improvement in diet-induced obesity mice. Mechanismly, anti-obesity effect of BTE depends on promoting BAT thermogenesis and WAT browning with upregulation of uncoupling protein 1 (UCP1), especially visceral adipose tissue (VAT) with browning resistance. Specifically, utilizing in silico approach of network pharmacology and molecular docking, we identified carbonic anhydrase 2 (CA2) in nitrogen metabolism as anti-obesity target of BTE and further elucidated that protein kinase B (AKT) signaling pathway linked CA2 and UCP1. Meanwhile gut microbiota regulation may prompt the CA2-dependent thermogenesis activation. Our findings demonstrated anti-obesity effect of BTE as thermogenic activator through CA2-mediated BAT thermogenesis and WAT browning via CA2-AKT-UCP1 signaling pathway, which could be developed as promising anti-obesity agent with good safety and efficacy.

Colorectal cancer (CRC) is the third most common and the second most fatal cancer. In recent years, more attention has been directed toward the role of gut microbiota in the initiation and development of CRC. Some bacterial species, such as Fusobacterium nucleatum, Escherichia coli, Bacteroides fragilis, Enterococcus faecalis, and Salmonella sp. have been associated with CRC, based upon sequencing studies in CRC patients and functional studies in cell culture and animal models. These bacteria can cause host DNA damage by genotoxic substances, including colibactin secreted by pks + Escherichia coli, B. fragilis toxin (BFT) produced by Bacteroides fragilis, and typhoid toxin (TT) from Salmonella. These bacteria can also indirectly promote CRC by influencing host-signaling pathways, such as E-cadherin/β-catenin, TLR4/MYD88/NF-κB, and SMO/RAS/p38 MAPK. Moreover, some of these bacteria can contribute to CRC progression by helping tumor cells to evade the immune response by suppressing immune cell function, creating a pro-inflammatory environment, or influencing the autophagy process. Treatments with the classical antibacterial drugs, metronidazole or erythromycin, the antibacterial active ingredients, M13@ Ag (electrostatically assembled from inorganic silver nanoparticles and the protein capsid of bacteriophage M13), berberine, and zerumbone, were found to inhibit tumorigenic bacteria to different degrees. In this review, we described progress in elucidating the tumorigenic mechanisms of several CRC-associated bacteria, as well as progress in developing effective antibacterial therapies. Specific bacteria have been shown to be active in the oncogenesis and progression of CRC, and some antibacterial compounds have shown therapeutic potential in bacteria-induced CRC. These bacteria may be useful as biomarkers or therapeutic targets for CRC.