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Objective: This study aims to investigate the therapeutic effect of Lactobacillus rhamnosus GG-loaded lemon pectin microspheres (LGG@LPM) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. Methods: LGG@LPM was characterized, and the therapeutic potential of gavage administration of LGG@LPM against UC in mice was explored. Results: LGG@LPM microspheres exhibited good stability. The administration of LGG@LPM significantly alleviated the pathological process of DSS-induced UC in mice, restoring normal body mass and colon length and decreasing histological activity index (HAI) and disease activity index (DAI). Additionally, LGG@LPM administration reversed the increase in inflammatory cytokine levels and the decrease in antioxidant enzyme activities in the colon, the increase in serum lipopolysaccharide (LPS) levels and the alterations in short-chain fatty acids (SCFAs) levels induced by DSS in mice. 16S rRNA sequencing revealed that LGG@LPM restored the gut microbiota in UC mice through enhancing the abundance of Lactobacillus and Mucispirillum, and the alteration of the microbiota was significantly correlated with some environmental factors. Conclusion: LGG@LPM could alleviate the pathological progression of UC by improving the gut microbiota, the effect being more pronounced than that of either lemon pectin or LGG alone.

Myricetin, a natural flavonoid found in various foods, was investigated for its antiviral effect against transmissible gastroenteritis virus (TGEV). This α-coronavirus causes significant economic losses in the global swine industry. The study focused on the papain-like protease (PLpro), which plays a crucial role in coronavirus immune evasion by mediating deubiquitination. Targeting PLpro could potentially disrupt viral replication and enhance antiviral responses. The results demonstrated that myricetin effectively inhibited TGEV-induced cytopathic effects in a dose-dependent manner, with an EC 50 value of 31.19 μM. Myricetin significantly reduced TGEV viral load within 48 h after an 8-h co-incubation period. Further investigations revealed that myricetin at a concentration of 100 μM directly inactivated TGEV and suppressed its intracellular replication stage. Moreover, pretreatment with 100 μM myricetin conferred a protective effect on PK-15 cells against TGEV infection. Myricetin competitively inhibited PLpro with an IC 50 value of 6.563 μM. Molecular docking experiments show that myricetin binds to the Cys102 residue of PLpro through conventional hydrogen bonds, Pi-sulfur, and Pi-alkyl interactions. This binding was confirmed through site-directed mutagenesis experiments, indicating myricetin as a potential candidate for preventing and treating TGEV infection., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Fan, Xi, Liu, Song, Zhao, Zhou, Zou, Fu, Li, Jia and Yin.)