The zebrafish (Danio rerio) has evolved into a strategic, high-throughput platform, bridging the critical gap between in vitro assays and costly mammalian studies in nanomedicine development. This is underscored by its prolific adoption, with over 1130 studies published in the last five years. The model's high genetic homology, optical transparency, and rapid development offer an ethically favorable system for the high-throughput assessment of nanotoxicity, biodistribution, and therapeutic efficacy. This review positions the zebrafish as an indispensable intermediate filter to prioritize lead candidates and deconvolute mechanistic pathways for nanomaterials. Critically, the model is best suited for preliminary in vivo evaluation; its findings necessitate subsequent validation in established mammalian models prior to any human translation. Systematically reviewing the literature, we organize nanomaterials by chemical composition and map their respective applications to different disease areas, analyzing the type of nanomaterial and its properties and therapeutic effectiveness. We detail how its integration with automated imaging, microinjection, and artificial intelligence (AI) is powering sophisticated high content screening pipelines, drastically reducing preclinical costs and timelines and with the possibility of developing personalized medicine. By improving predictive validity and serving as a bridge between in vitro trials and preclinical studies in higher-order animals, the zebrafish model streamlines the translation pathway, accelerating the development of therapies within the nanoworld.

Trishizukaol A alleviates chronic kidney disease by restraining P2X7/PSME3-driven 20S proteasome hyperactivation.

Inhibition of the p38/JNK MAPK pathway mediated by circadian rhythm genes: Study of the mechanism of Linggan Wuwei Jiangxin decoction in the treatment of COPD.

Long Gu (Os Draconis): Textual research, modern scientific evaluation, and quality control challenges.

BACKGROUND Ulcerative colitis (UC) is a chronic inflammatory bowel disease for which effective therapies are lacking. Niu Huang (NH) is a traditional Chinese medicine used for inflammatory disorders. However, its protective effect on UC and its underlying mechanisms are unknown. AIM To uncover the mechanisms underlying the anti-colitis effects of the NH. METHODS Network pharmacology was applied to predict the active ingredients and targets of NH. Experimental validation was conducted in a dextran sulfate sodium-induced murine colitis model. The therapeutic efficacy was assessed using symptoms, histopathology, quantitative polymerase chain reaction, western blotting, immunohistochemistry and enzyme linked immunosorbent assay, while the underlying mechanism was investigated through integrated transcriptomic and proteomic analyses. In addition, the critical role of farnesoid X receptor (FXR) in mediating the effects of NH was validated using the FXR inhibitor guggulsterone and Fxr-/- mouse models. RESULTS Network pharmacology revealed that the bioactive component of NH is bile acid. Our animal experiments demonstrated that NH treatment significantly alleviated colitis symptoms and pathological damage. NH preserved intestinal mucosal integrity by upregulating occludin, claudin3, E-cadherin and leucine rich repeat containing G protein-coupled receptor 5 expression. Transcriptomic and proteomic analyses revealed that bile secretion, the nuclear factor kappa B signaling pathway and the complement and coagulation cascade pathway are key targets of NH. Western blotting confirmed that NH increased FXR levels and reduced P65, complement component 3 (C3) and NOD-like receptor family pyrin domain containing 3 (NLRP3) expression. Furthermore, experiments using Fxr -/- mice and the FXR antagonist revealed that FXR is a pivotal target through which NH attenuates UC. Mechanistic analysis revealed that the effects of NH on UC are mediated by the modulation of targets involved in the activation of FXR and the subsequent inhibition of C3/NLRP3 activation. CONCLUSION This study demonstrates the therapeutic effects of NH on UC. Mechanistically, NH acts by activating FXR, which subsequently inhibits the nuclear factor kappa B pathway to reduce C3 accumulation and suppress excessive NLRP3 inflammasome activation in colon tissue.

Integrating transcriptomics and metabolomics to explore the therapeutic effects and mechanisms of Zhushagen-Shandougen herb pair on chronic pharyngitis.

Ophiopogonin D reprograms the polarization of macrophages through modulating PPM1K-mediated branched-chain amino acids catabolism to delay atherogenesis.

Plant-derived bioactive compounds attenuate acute lung injury by regulating cellular autophagy and inflammation: A review.

Therapeutic mechanisms of natural plant polysaccharides in ulcerative colitis: A review.

Synthesis and pharmacological evaluation of brominated derivatives of natural product celastrol for treatment of hepatic fibrosis.

Hedyotis diffusa Willd. extract alleviates CCl4-induced liver fibrosis via modulation of the gut microbiota and FXR/SHP/CYP7A1-mediated bile acid metabolism.

Therapeutic potential of Isatidis Radix alkaloids in RSV pneumonia: A focus on AhR-mediated pulmonary barrier repair.

Xuefu Zhuyu decoction attenuates thoracic aortic dissection by regulating VSMC phenotypic switching and oxidative stress via the JAK2/STAT3/HIF-1α pathway.

Zha-Chong Shi-San-Wei Pill inhibits ferroptosis in cerebral ischemia via bioinformatics and experimental confirmation methods.

Combining LC/IM-QTOF-MS with serum pharmacochemistry to identify active compounds and functional mechanisms of Fritillaria ussuriensis in asthma.

Haikun Shenxi Capsule alleviates Alzheimer's disease by targeting mitophagy to clear turbidity toxin.

ShenRongGuBenHuanShao Pill ameliorates oligoasthenospermia by alleviating oxidative stress and DNA damage via activation of the PI3K/Akt/mTOR pathway.

Anlotinib+Toripalimab maintenance in Extensive-Stage small cell lung Cancer: Clinical efficacy and preclinical mechanism of anlotinib-induced neuroendocrine differentiation Suppression via Notch1.

Mo2C nanozyme targets citrate synthase to treat acute kidney injury through alleviating oxidative stress and dysfunction of energy metabolism.

Licorice (Gancao in Chinese, GC), a traditional antidote with "universal detoxifying" properties, has been reported to promote uranium excretion via glycyrrhizic acid (GL) and demonstrate significant efficacy against acute uranium damage. However, the underlying mechanisms remain largely unclear. This study employed a metabolomics approach combining respiratory analysis with gas chromatography-mass spectrometry to evaluate the reparative effects of licorice extract (LE) on acute uranium injury. A high-performance liquid chromatography (HPLC) method was used to determine the content of glycyrrhizic acid in licorice. After 7 days of administration, rat body weight and peripheral blood parameters showed significant recovery. Breath metabolomics identified eight differentially expressed metabolites, whereas serum metabolomics revealed 17 metabolites associated with acute uranium injury. Metabolic pathway analysis indicated that LE primarily exerted its restorative effects through four key pathways in respiratory metabolomics and five key pathways in serum metabolomics. Glycine, serine, and threonine metabolism were observed as common metabolic pathways in both exhaled breath and serum metabolomics, showing the strongest association with LE's repair of acute uranium damage. This study demonstrates that LE effectively ameliorates acute uranium damage, and metabolomics serves as a powerful tool for deepening understanding of traditional Chinese medicine's therapeutic effects on acute uranium injury.