Zhongwei Zhang

Glutinous rice huangjiu, a non-distilled wine variety unique to China, is rich in nutrients. However, systematic research on the differences in its non-volatile functional components remains scarce, despite these variations being key factors influencing its antioxidant effects. This study employed non-targeted metabolomics to systematically analyze the non-volatile metabolite profiles of 16 glutinous rice huangjiu brands, identifying 1450 metabolites. An alcohol-induced hepatocyte injury model was established, combining cell viability and reactive oxygen species (ROS) level assays to screen for samples (G10 and G11) exhibiting significant efficacy across varying alcohol concentrations. Differential metabolite analysis further identified key bioactive compounds including L-proline, dihydroferulic acid, chalcones, and multiple phenolic derivatives. Using molecular docking technology, we preliminarily revealed that these components may exert antioxidant and hepatoprotective effects either by directly scavenging free radicals or indirectly through mechanisms such as participating in glutathione metabolism and regulating the KEAP1-Nrf2 signaling pathway. This study elucidates the differences among glutinous rice huangjiu at the metabolomic and cellular model levels, providing a scientific basis for evaluating the health benefits and developing new products of huangjiu.

Pingyin rose essential oil (PREO) is extracted from fresh petals exclusively cultivated in Shandong Province. This PREO has been used in traditional Chinese medicine (TCM) for decades to treat skin issues like excessive oxidative stress and inflammation. The purpose of this study was to assess the impact of PREO on the inflammatory pathway in HaCaT cells produced by LPS. In vitro methods were used to ascertain the expression of inflammatory proteins, and network pharmacological analysis was employed to predict the signaling pathway. According to our findings, PREO significantly reduced LPS-induced oxidative stress, decreasing nitric oxide (NO) and reactive oxygen species (ROS) production by 42% and 38%, respectively, and malondialdehyde (MDA) levels by 35%, while enhancing superoxide dismutase (SOD) activity by 28% (p < 0.01). PREO treatment (0.1%, 18 h) markedly suppressed pro-inflammatory cytokines, with mRNA levels of TNF-α, IL-1β, IL-6, and IL-8 reduced by 52%, 47%, 45%, and 40%, respectively. Mechanistically, PREO inhibited the TLR4-NF-κB pathway, downregulating MyD88 and TRIF expression by 60% and 55%, and reducing NF-κB p65 and IκB-α phosphorylation by 50% and 48%. Network pharmacology and molecular docking identified Citronellol (54.37% of PREO) as the major bioactive component, exhibiting strong binding affinities with IKKβ (−5.7 kcal/moL) and MyD88 (−4.5 kcal/moL). This research, distinct from previous investigations on Rosa rugosa polyphenols, provides a novel mechanistic link between PREO’s traditional use and its observed anti-inflammatory and antioxidant effects in keratinocytes, specifically through inhibition of the TLR4-NF-κB pathway.

Bacterial extracellular vesicles (EVs) play a pivotal role in host–microbe communication. Akkermansia muciniphila, a symbiotic bacterium essential for intestinal health, is hypothesized to exert its effects via EVs. Here, we successfully isolated and characterized EVs derived from A. muciniphila (Am-EVs) using ultracentrifugation. Am-EVs exhibited a double-membrane structure, with an average diameter of 92.48 ± 0.28 nm and a proteomic profile comprising 850 proteins. In an in vitro model of lipopolysaccharide (LPS)-induced inflammation in human colorectal adenocarcinoma cells (Caco-2), treatment with both 25 and 50 μg/mL Am-EVs significantly reduced oxidative stress markers, including reactive oxygen species (ROS), nitric oxide (NO), and malondialdehyde (MDA), while restoring catalase activity (CAT). Am-EVs also suppressed the expression of pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). Subsequent transcriptomic sequencing and Western blot experiments revealed that Am-EVs attenuate the MAPK signaling pathway by downregulating TRIF, MyD88, p38 MAPK, and FOS while upregulating TGFBR2. These findings suggest that Am-EVs mediate anti-inflammatory effects through modulation of MAPK signaling, highlighting their potential as therapeutic agents in intestinal inflammation.