地榆炭纳米类成分对溃疡性结肠炎的保护作用及机制研究OA

This study aims to isolate and extract Sanguisorbae Radix Carbonisata nano-components(SRC-NCs)from Sanguisorbae Radix Carbonisata(SRC)and investigate their protective effects against ulcerative colitis(UC)and the underlying mechanisms.The SRC-NCs were systematically characterized by nanomaterial characterization techniques to analyze their morphological structure,optical properties,and characteristics of functional groups on the surface.Meanwhile,a dextran sulfate sodium(DSS)-induced UC mouse model was established to evaluate the general condition,disease activity index(DAI)score,and pathological damage degree of the colon tissue of mice after SRC-NCs intervention.The level or activity of inflammatory factors(interleukin(IL)-17A,IL-6,IL-10,IL-2,tumor necrosis factor alpha(TNF-α),and IL-1β)and oxidative stress markers(myeloperoxidase(MPO),malondialdehyde(MDA),superoxide dismutase(SOD),glutathione(GSH),and nitric oxide(NO))in the colon tissue was detected.The expression level of key proteins,such as Toll-like receptor 4(TLR4),myeloid differentiation primary response protein 88(MYD88),and nuclear factor-kappa B p65(NF-κB p65),in the colon tissue was detected by Western blot to provide key molecular evidence for revealing the intervention mechanism of SRC-NCs.The results showed that SRC-NCs were nearly spherical under transmission electron microscope(TEM),with a uniform particle size distribution(0.8-2.6 nm),a lattice spacing of 0.17 nm,and multiple active genes such as hydroxyl,amino,and carboxyl groups on the surface.In the UC model,SRC-NCs could slow down the weight loss and increase in DAI score of mice,and alleviate the shortening of the colon and the degree of tissue damage.SRC-NCs could down-regulate the levels of pro-inflammatory factors such as IL-17A,IL-6,IL-2,TNF-α,and IL-1β in the colon tissue,up-regulate the level of anti-inflammatory factor IL-10,reduce the activity of MPO and the content of MDA and NO,increase the activity of SOD and the level of GSH,and inhibit the expression of TLR4/MYD88/NF-κB p65 proteins.In conclusion,the study for the first time demonstrates that SRC-NCs are the key active components of SRC in exerting protective effects against UC,and the mechanism may be related to the inhibition of inflammatory responses of the TLR4/MYD88/NF-κB pathway and the reduction of oxidative stress.