Ulcerative colitis (UC) has been identified as one of the inflammatory diseases. Intestinal mucosal barrier function and microflora play major roles in UC. Modified-chitosan products have been consumed as effective and safe drugs to treat UC. The present work aimed to investigate the effect of chitosan (CS) on intestinal microflora and intestinal barrier function in dextran sulfate sodium (DSS)-induced UC mice and to explore the underlying mechanisms. KM (Kunming) mice received water/CS (250, 150 mg/kg) for 5 days, and then received 3% DSS for 5 days to induce UC. Subsequently, CS (250, 150 mg/kg) was administered daily for 5 days. Clinical signs, body weight, colon length, and histological changes were recorded. Alterations of intestinal microflora were analyzed by PCR-DGGE, expressions of TNF-α and tight junction proteins were detected by Western blotting. CS showed a significant effect against UC by the increased body weight and colon length, decreased DAI (disease activity index) and histological injury scores, and alleviated histopathological changes. CS reduced the expression of TNF-α, promoted the expressions of tight junction proteins such as claudin-1, occludin, and ZO-1 to maintain the intestinal mucosal barrier function for attenuating UC in mice. Furthermore, Parabacteroides, Blautia, Lactobacillus, and Prevotella were dominant organisms in the intestinal tract. Blautia and Lactobacillus decreased with DSS treatment, but increased obviously with CS treatment. This is the first time that the effect of original CS against UC in mice has been reported and it is through promoting dominant intestinal microflora such as Blautia, mitigating intestinal microflora dysbiosis, and regulating the expressions of TNF-α, claudin-1, occludin, and ZO-1. CS can be developed as an effective food and health care product for the prevention and treatment of UC.

Tumor-specific combination therapy has shown great promise in cancer theranostics. However, the therapeutic efficacy is usually suppressed because most of the therapeutic systems are not able to synchronously activate their different therapeutic approaches and the local concentration of tumorassociated stimulus is generally insufficient to fully activate the combination therapy process. Herein, a MnO 2 -doped CeO 2 nanozyme-based nanomedicine (Ce6@CMNRs) is reported for tumor-specific synchronously activated chemodynamic/photodynamic combination therapy. The tumor-overexpressed H 2 O 2 substitutes the Ce6 on Ce6@CMNRs surfaces via competitive coordination and then decomposes into •OH under acidic condition, achieving the chemodynamic therapy (CDT). Meanwhile, the substituted Ce6 triggers photodynamic therapy (PDT) under laser irradiation that is suppressed before the substitution occurs. Thus, H 2 O 2 can synchronously activate both CDT and PDT of Ce6@CMNRs with a similar level in tumor sites. Moreover, the activated PDT-induced oxygen starvation further triggers the generation of H 2 O 2 to continuously replace the residual Ce6 coordinated on the nanorod surface, thereby leading to the full activation of PDT and CDT. Also, the doped MnO 2 enhances the generation of •OH and provides high contrast for magnetic resonance imaging (MRI) with the help of glutathione. Therefore, Ce6@CMNRs are promising candidates for MRI-guided CDT/PDT combination therapy with minimized side effects and high efficiency.

Chemodynamic therapy (CDT) is a kind of novel cancer treatment with minimized side effects. As the therapeutic efficacy of a single CDT is usually not satisfactory, combining other therapeutic modalities...

We report a nanoenzyme-based photothermal agent, in which the nanoenzyme acts as a peroxidase, prodrug carrier, and MRI contrast agent. The formation of dimer by the prodrug under the catalysis...