Arctigenin

Arginine (ARG) improves meat quality and fat deposition; however, its effects on gut microbiota-mediated lipid metabolism in lambs remain unclear. Twenty-four lambs were divided into control (fed a basal diet) and ARG groups (with 1 % ARG added). In the ARG group, backfat thickness, shear force in the longissimus thoracis (LT) muscle, and C16:0 and SFA contents in the subcutaneous adipose tissue (SAT) were reduced, whereas the eye muscle area, a* value, and intramuscular fat, C18:2n-6c, C20:4n-6, C20:5n-3, and PUFA contents in the LT were elevated. Moreover, the ARG group exhibited higher levels of Prevotella, Akkermansia, Faecalibacterium, SCFAs, and GLP-1 in the colon, and lower serum triglyceride and glucose levels. Interestingly, ARG differentially regulated lipid metabolism in the SAT and LT via the GLP-1R/AMPK and triglyceride metabolism signalling pathways. Overall, ARG addition may optimise gut microbiota composition, fat deposition, and meat quality, providing application guidance for regulating fat deposition in lambs.

Hepatocellular carcinoma (HCC) is a predominant malignant liver tumor that cannot be efficiently treated because of poor response, toxicity, and drug resistance. Ferroptosis is an iron-dependent way of cell death associated with abnormal intracellular lipid metabolism. Celastrol (Cel) has the ability to inhibit the progression of HCC by regulating multiple signaling pathways and induce ferroptosis. However, Cel exists the limitations of low water solubility, low oral bioavailability, and high organ toxicity. Cel was encapsulated in polyethylene glycol-based liposomes modified with L-arginine (Cel@Lip-Arg). Cel@Lip-Arg has a uniform size distribution (∼100 nm), high drug loading (80 %), and excellent ability to target liver cancer cells. In vitro experiments demonstrated that Cel@Lip-Arg considerably suppressed the activity of HuH7 (hepatoma) cells but had a negligible effect on L02 (normal) cells. Cel@Lip-Arg induced ferroptosis in hepatoma cells by promoting transferrin receptor expression, inhibiting system xc^- and glutathione peroxidase 4, and favoring intracellular peroxide accumulation. In vivo experiments revealed that Cel@Lip-Arg plays a therapeutic role by inducing ferroptosis. Compared to Cel, Cel@Lip-Arg had a higher anti-hepatoma activity and effectively reduced the toxicity of Cel in mice. Cel@Lip-Arg-induced ferroptosis was concluded to be an attractive strategy for the precise treatment of HCC.