Ying Xu

Camellia oleifera seed cake is a major byproduct of the oil industry, often underutilized despite its richness in bioactive compounds. This study investigated the therapeutic effects and underlying mechanisms of C. oleifera seed cake extract (SCE) on potassium oxonate/hypoxanthine‐induced hyperuricemia and renal injury in mice. SCE administration significantly reduced serum uric acid levels and improved renal function parameters (creatinine and blood urea nitrogen). Mechanistically, SCE inhibited hepatic xanthine oxidase and adenosine deaminase activities and modulated renal urate transporters by downregulating URAT1 and GLUT9 while upregulating OAT1 and ABCG2, thereby inhibiting uric acid synthesis and facilitating its excretion. UHPLC–MS/MS analysis identified 134 chemical constituents in SCE, primarily phenylpropanoids and polyketides. Integrated network pharmacology predicted the involvement of inflammatory pathways, which was validated in vivo. The results confirmed that SCE alleviated renal oxidative stress and inflammation by activating the Nrf2/Keap1 signaling pathway and suppressing the NLRP3 inflammasome. These findings demonstrate that SCE exerts potent anti‐hyperuricemic and nephroprotective effects through multi‐target regulation, supporting its potential as a functional food ingredient.

Chrysoeriol is a flavonoid with anti-inflammatory and antioxidant capacities against inflammatory diseases. Inflammation and apoptosis participate in the pathogenesis of cisplatin-induced nephrotoxicity. The role of chrysoeriol on acute kidney injury in a cisplatin induced rat model was investigated in this study. An evaluation of the effect of chrysoeriol on cisplatininduced nephrotoxicity by measuring histopathological changes and proinflammatory biomarkers revealed activation of PI3K/AKT and inactivation of NF-κB pathways in the reno-protection by chrysoeriol.

Brucea javanica oil (BJO) is beneficial for the treatment of ulcerative colitis (UC), and that quassinoids in particular brusatol are bioactive components. However, it is still uncertain whether or not other components in BJO, such as oleic acid and fatty acids, have an anti‐UC effect. The present study is aimed at comparing the anti‐UC effects between brusatol‐enriched BJO (BE‐BJO) and brusatol‐free BJO (BF‐BJO) and at exploring the effects and mechanisms of BE‐BJO on colon inflammation and intestinal epithelial barrier function. Balb/C mice received 3% (wt/vol) DSS for one week to establish the UC model. Different doses of BE‐BJO, BF‐BJO, or BJO were treated. The result illustrated that BE‐BJO alleviated DSS‐induced loss of body weight, an increase of disease activity index (DAI), and a shortening of colon, whereas BF‐BJO did not have these protective effects. BE‐BJO treatment improved the morphology of colon tissue, inhibited the production and release of TNF‐α, IFN‐γ, IL‐6, and IL‐1β in the colon tissue, and reversed the decreased expressions of ZO‐1, occludin, claudin‐1, and E‐cadherin induced by DSS but augmented claudin‐2 expression. Mechanistically, BE‐BJO repressed phosphorylation of NF‐κB subunit p65, suppressed RhoA activation, downregulated ROCK, and prevented phosphorylation of myosin light chain (MLC) in DSS‐treated mice, indicating that the protective effect of BE‐BJO is attributed to suppression of NF‐κB and RhoA/ROCK signaling pathways. These findings confirm that brusatol is an active component from BJO in the treatment of UC.