Corrigendum: Lycium barbarum Glycopeptide prevents the development and progression of acute colitis by regulating the composition and diversity of the gut microbiota in mice.

[This corrects the article DOI: 10.3389/fcimb.2022.921075.].

Lycium barbarum Glycopeptide prevents the development and progression of acute colitis by regulating the composition and diversity of the gut microbiota in mice.

In most cases, recurrent chronic colitis is caused by the recurrence of acute colitis after incomplete recovery and re-exposure to irritating factors, and the gut microbiome, which is the largest micro-ecosystem in the human body, plays a crucial role in the development of colitis. Plant polysaccharides have always been reported to have the ability for anti-inflammation, and they are closely related to the gut microbiome. Lycium barbarum Glycopeptide (LbGP), the most potent component obtained by further isolation and purification from Lycium barbarum fruit, has been shown to inhibit inflammation in animal models. However, its therapeutic efficacy in colitis and its mechanism in gut microbiota regulation have not been fully studied. In our study, the dextran sulfate sodium (DSS)-induced mouse model was used to dynamically evaluate the effect of LbGP in the treatment of acute colitis and the mechanism from the perspective of the gut microbiome through the 16S rDNA sequence. The results showed that LbGP treatment significantly alleviated acute colitis and improved the gut microbiome compared with that in the model group. Harmful bacteria, such as Lachnoclostridium spp. and Parabacteroides_distasonis, were inhibited and probiotics, such as Bacteroides_acidifaciens, Lactobacillus spp., Turicibacter spp., and Alistipes spp., were increased by LbGP treatment. Further, a Random Forest analysis with 10-fold cross-validation identified a family named Muribaculaceae representing colitis development and recovery upon LbGP treatment. In conclusion, our study demonstrated the capability of LbGP to prevent the development of acute colitis by regulating the composition and diversity of the gut microbiota and highlighted the dynamic process of gut microbiota with the colitis progression. Further, it provides evidence to develop LbGP as a functional food supplement and future drug acting on intestinal disease.

Modulation of expression of p16 and her2 in rat breast tissues of mammary hyperplasia model by external use of rupifang extract.

OBJECTIVE: To observe the effect of Rupifang Extract in external use on expression of proto-oncogenes her2 and tumor suppression genes p16 in rat breast tissues of mammary hyperplasia model. To explore the mechanisms of Rupifang Extract in external use for preventing and treating mammary hyperplasia. METHODS: Thirty virginal female Wistar rats were randomized into 5 groups, 6 in each, A: blank control group; B: model group; C: the low dose group of Rupifang; D: the middle dose group of Rupifang; and E: The high dose group of Rupifang. The mammary hyperplasia rat models were produced by injecting estradiol benzoate and progesterone and irritating by tail nipping. Drug intervention was also launched during the model formation. After 30 days, the expression of her2 and p16 in breast tissues of rats in each group were detected by the SP immunohistochemical method. RESULTS: Compared with Blank control group, the expression of her2 in breast tissues in Model group was higher, and the expression of p16 was lower (P < 0.05 or P < 0.01). After intervention with Rupifang Extract, compared with Model group, the expression of her2 in breast tissues in Rupifang groups was lower, and the expression of p16 higher (P < 0.05 or P < 0.01). CONCLUSION: The mechanisms of Rupifang Extract in external application for preventing and treating mammary hyperplasia may be reducing the expression of proto-oncogenes her2 and increasing the expression of tumor suppression genes p16.