# Miniature rose alleviates inflammatory bowel disease in mice by modulating gut microbiota, inhibiting TLR4, enhancing tight junction proteins, and promoting metabolism

## TL;DR

Miniature rose extract helps treat inflammatory bowel disease in mice by improving gut health, reducing inflammation, and balancing gut bacteria.

## Contribution

This study identifies the multi-target therapeutic potential of Miniature Rose extract in treating IBD through gut microbiota modulation and intestinal barrier restoration.

## Key findings

- MR extract reduced DSS-induced colitis by upregulating tight junction proteins Occludin and ZO-1.
- MR modulated gut microbiota by increasing Bacteroides and Alloprevotella while decreasing Erysipelatoclostridium.
- MR inhibited inflammatory proteins TLR4 and TLR9 and corrected metabolic dysregulation in IBD.

## Abstract

Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disorder of the gastrointestinal tract. Its pathogenesis is complex and not fully understood, so it remains incurable. Traditional Chinese medicine (TCM) attracts attention as a potential option. It offers multi-target actions. This study investigated the protective effects of an aqueous extract of Miniature Rose (MR), a medicinal plant from Xinjiang, in a dextran sulfate sodium (DSS)-induced murine model of IBD. We focused on gut microbiota, intestinal barrier integrity, and metabolic homeostasis.

IBD was induced in mice by DSS, followed by intervention with different doses of aqueous MR extract. A multi-faceted approach incorporating 16S rRNA sequencing, non-targeted metabolomics, immunohistochemistry, and ELISA was used to evaluate the effects of MR on gut microbiota composition, fecal metabolic profiles, intestinal barrier protein expression, and the expression of the inflammatory proteins TLR4 and TLR9.

Treatment with aqueous MR extract markedly alleviated DSS-induced colitis. MR improved intestinal barrier integrity by upregulating the tight junction proteins Occludin (OCC) and Zonula Occludens-1 (ZO-1), while concurrently downregulating TLR4 and TLR9. MR administration also markedly modulated the gut microbiota, increasing the relative abundance of beneficial genera (Bacteroides and Alloprevotella) and decreasing the abundance of the pathobiont Erysipelatoclostridium. In addition, MR mitigated the metabolic dysregulation observed in DSS-induced colitis.

MR ameliorates DSS-induced colitis through a multifaceted mechanism that involves coordinated regulation of the gut microbiota, restoration of the intestinal barrier, inhibition of inflammatory protein expression, and correction of metabolic dysregulation. These findings highlight the potential of MR as a multi-target therapeutic candidate and provide an experimental basis for its further preclinical and clinical evaluation in IBD.