Quercetin (QT) is a plant polyphenol with various pharmacological properties. However, the low water solubility limits its therapeutic efficacy. In the present study, QT-loaded sodium taurocholate-Pluronic P123 (QT-loaded ST/P123) mixed micelles were developed and characterized, and the effect of the formulation on improving the water solubility of QT was investigated. QT-loaded ST/P123 mixed micelles were prepared by thin film hydration-direct dissolution and optimized by uniform design. The optimal formulation possessed high drug loading (12.6%) and entrapment efficiency (95.9%) in small (16.20 nm) spherically-shaped micelles. A low critical micelle concentration indicated that the micelles were stable, and they showed a sustained release pattern, as determined in vitro in simulated gastric fluid and intestinal fluid. Pharmacokinetic evaluation showed the C and AUC were 1.8-fold and 1.6-fold higher than the QT suspension. The present results indicate that QT-loaded ST/P123 micelles are potential candidates to improve the solubility and oral bioavailability of QT.

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Background Ulcerative colitis (UC) is an inflammatory bowel disease that causes continuous mucosal inflammation. Anemonin is a natural molecule from the Ranunculaceae and Gramineae plants that exerts anti-inflammatory properties. This study aimed to explore the effects and mechanisms of anemonin on UC. Methods C57BL/6 mice were administered dextran sulphate sodium (DSS; 3% [w/v]) to establish an animal model of UC. Mice were treated with an intraperitoneal injection of anemonin. Body weight and the disease activity index (DAI) were recorded. Haematoxylin and eosin staining, RT-qPCR, ELISA, and western blotting were performed to evaluate the histopathological changes and tissue inflammation. HT-29 cells were treated with lipopolysaccharide (LPS) and anemonin. Cell inflammation was evaluated using RT-qPCR and western blotting. The target proteins of anemonin were predicted using bioinformatics analysis and confirmed in vitro and in vivo. Results Anemonin improved DSS-induced body weight loss, shortened colon length, increased DAI, and induced pathological changes in the colon tissue of mice. Anemonin inhibited DSS-induced colon tissue inflammation as the release of IL-1β, TNF-α, and IL-6 was significantly suppressed. Additionally, anemonin attenuated LPS-induced cytokine production in HT-29 cells. PKC-θ was predicted as a target protein of anemonin. Anemonin did not affect PRKCQ gene transcription, but inhibited its translation. PRKCQ overexpression partially reversed the protective effects of anemonin on HT-29 cells. Adeno-associated virus delivery of the PRKCQ vector significantly reversed the protective effects of anemonin on the mouse colon. Conclusions Anemonin has the potential to treat UC. The anti-inflammatory effects of anemonin may be mediated through targeting PKC-θ.