Proanthocyanidins (PACs) have been proven to exert antioxidant and anti-inflammatory effects. In this study, ultra-performance liquid chromatography (UPLC) coupled with linear ion trap-Orbitrap (LTQ-Orbitrap) high-resolution mass spectrometry was first employed to systematically screen PACs from the roots of Ephedra sinica Stapf, and its ethyl acetate extract (ERE) was found to contain PAC monomers and A-type dimeric proanthocyanidins, which were tentatively identified through characteristic fragmentation patterns. In vitro, the antioxidant activity of ERE was tested through 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2, 2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) assays. In addition, ERE could inhibit the production of nitric oxide (NO) in lipopolysaccharide (LPS)-induced RAW 264.7 cells. In vivo, the preventative effects on dextran-sulfate-sodium-induced ulcerative colitis in mice was investigated. Mice were administered with ERE for 21 days, and during the last 7 days of the treatment period dextran sulfate sodium (DSS) was used to induce experimental colitis. The results showed that ERE treatment alleviated DSS-induced colitis, which was characterized by decreases in disease activity index (DAI) scores, spleen index and colon levels of TNF-α and IL-6, mitigation in pathological damage and oxidative stress and increases in colon length and IL-10 levels. In conclusion, supplementation of PACs derived from ERE may offer a new strategy for the treatment of ulcerative colitis. Moreover, our research will greatly facilitate better utilization of Ephedra plants.

The study aimed to optimize the processing conditions of Gardeniae Fructus with ginger juice (GFPG) and confirm its therapeutic effects and pharmacological mechanisms on cholestatic liver injury. Processing conditions were optimized using response surface methodology (RSM) and thermal analysis, focusing on geniposide content as a key active compound. Variables included processing time, moistening time, and the solid-liquid ratio. Optimal conditions were: ginger juice to Gardeniae Fructus ratio of 8:1 (w/v), processing temperature of 208 °C, moistening time of 3 hours, and processing time of 5 minutes. Pharmacological mechanisms were analyzed through network pharmacology, molecular docking, and experimental validation using alpha-naphthyl isothiocyanate (ANIT)-induced cholestatic liver injury in mice and lipopolysaccharide (LPS)-stimulated RAW264.7 cell models. In vivo, GFPG extract alleviated ANIT-induced cholestatic liver injury by improving liver function markers (AST, ALT, TBA, TBIL, DBIL) and modulating TLR4/NF-κB, FXR/PPAR-α, and PI3K/AKT/GSK-3β pathways. In vitro, it reduced LPS-induced production of inflammatory mediators (NO, TNF-α, IL-6, IL-1β) through TLR4/NF-κB pathway inhibition. This study established optimal processing methods for GFPG using RSM and thermal analysis, providing robust quantitative parameters. GFPG demonstrated significant therapeutic effects in cholestatic liver injury models, indicating its potential as a candidate for developing treatments for cholestatic hepatitis.

Rheumatoid arthritis (RA) is characterized by systemic inflammation and synovial hyperplasia. Pristimerin, a natural triterpenoid isolated from plants belonging to the Celastraceae and Hippocrateaceae families, has been reported to exhibit anti-inflammation and anti-proliferation activities. Our study aims to reveal the antiarthritic effects of pristimerin and explore its potential mechanism using in vitro, in silico, and in vivo methods. In the present study, pristimerin treatment led to a dose-dependent decrease in cell viability and migration in TNF-α stimulated human rheumatoid arthritis fibroblast-like synoviocytes MH7A. Moreover, UPLC-LTQ-Orbitrap-based cell metabolomics analysis demonstrated that phospholipid biosynthesis, fatty acid biosynthesis, glutathione metabolism and amino acid metabolic pathways were involved in TNF-α induced MH7A cells after pristimerin treatment. In addition, the adjuvant–induced arthritis (AIA) rat model was employed, and the results exhibited that pristimerin could effectively relieve arthritis symptoms and histopathological damage as well as reduce serum levels of TNF-α, NO and synovial expressions of p-Akt and p-Erk in AIA rats. Furthermore, network pharmacology analysis was performed to visualize crucial protein targets of pristimerin for RA treatment, which showed that the effects were mediated through the MAPK/Erk1/2, PI3K/Akt pathways and directing binding with TNF-α. Taken together, our study not only offered new insights into the biochemical mechanism of natural compounds for RA treatment, but also provided a strategy that integrated in vitro, in silico and in vivo studies to facilitate screening of new anti-RA drugs.

Ussurian pear extract alleviates acute alcoholic liver injury by enhancing ethanol metabolism, activating the KEAP1/Nrf2/HO-1 antioxidant pathway, and inhibiting NF-κB/MAPK-mediated inflammation.

Background: Obesity-associated skeletal muscle atrophy is characterized by reduced muscle mass with excessive adipose accumulation, and there is no approved pharmacological therapy targeting both muscle anabolism and lipid metabolism. The root part of Ophiopogon japonicus (OJ), an edible traditional medicine (Liriopis seu Ophiopogonis Tuber), exhibits anti-diabetic, anti-inflammatory, and cardioprotective properties, yet its impact on obesity-associated muscle atrophy remains unknown. Methods: This study investigated the therapeutic potential and mechanisms of OJ extract against muscle atrophy in high-fat diet (HFD)-induced obesity mice and palmitate (PA)-stimulated C2C12 myotubes. Results: In obese mice, the administration of OJ extract inhibited muscle loss, improved muscle strength, and attenuated hepatic steatosis and dyslipidemia. Furthermore, OJ treatment restored myotube diameter, increased the expression of MyHC and Myogenin, and suppressed the expression of Atrogin-1 and MuRF1 in C2C12 myotubes. At the molecular level, OJ extract activated the PI3K-AKT-mTOR/FoxO3a signaling pathway and reprogrammed lipid metabolism in gastrocnemius tissues and myotubes. Conclusions: OJ extract alleviates obesity-induced muscle atrophy through regulation of the PI3K-AKT-mTOR/FoxO3a signaling pathway and lipid metabolism in muscle, indicating its potential as a natural therapeutic agent for obesity-associated muscle atrophy.

Background: Sarcopenic obesity (SO) is a metabolic myopathy characterized by the coexistence of obesity and decline of muscle mass and function. Obesity-related muscle atrophy represents a central pathological feature of this condition. Polygonati Rhizoma is widely used as a dietary herb with tonic effects in traditional Asian medicine. This study aims to investigate the effects and underlying molecular mechanisms of the water extract of Polygonati Rhizoma (WPR) on obesity-related muscle atrophy. Methods: The effects and potential mechanisms of WPR were explored using an obesity-induced muscle atrophy (OIMA) mouse model, palmitic acid (PA)- or lipopolysaccharide (LPS)-induced myotube atrophy models, and a myogenic differentiation model in C2C12 cells. Results: In OIMA mice, WPR attenuated obesity-related skeletal muscle atrophy and improved muscle strength and endurance. In the gastrocnemius muscle, WPR-treated mice showed lower levels of oxidative stress and inflammation, increased markers of mitochondrial biogenesis, and an improved balance between protein synthesis and degradation. In PA- or LPS-induced myotube atrophy models, WPR treatment suppressed the ubiquitin–proteasome system (UPS)-mediated proteolysis and NFκB/MAPK-related inflammatory signaling. In addition, WPR promoted myogenic differentiation in C2C12 myoblasts, which was associated with regulation of the p38 MAPK/MyoD/Myogenin axis. Conclusions: Our study suggests that WPR exerts a potential mitigating effect on obesity-related muscle atrophy, and this effect may be associated with the modulation of skeletal muscle inflammatory signaling, mitochondrial function, and protein metabolic balance. These findings are exploratory and provide mechanistic clues for future research aimed at developing potential intervention strategies for obesity-related muscle atrophy.