# Xuebijing injection mitigates instant blood−mediated inflammatory reaction and enhances intrahepatic islet transplantation via target NF−κB pathway

**Authors:** Yixiang Zhan, Yingbo Wang, Boya Zhang, Yijun Zhang, Rui Liang, Jiuxia Yang, Tengli Liu, Xiaoyan Hu, Tianyi You, Na Liu, Yuqi Chen, Qing Liu, Tingsheng Jiang, Zhaoce Liu, Xiangheng Cai, Runnan Yang, Yingyi Qi, Peng Sun, Jiaqi Zou, Xuejie Ding, Zhuzeng Yin, Shusen Wang

PMC · DOI: 10.3389/fimmu.2025.1671966 · Frontiers in Immunology · 2025-12-23

## TL;DR

Xuebijing injection reduces inflammation during islet transplantation, protecting islets and improving transplant success by targeting the NF-κB pathway.

## Contribution

Xuebijing is shown to mitigate IBMIR and enhance islet transplantation outcomes through dual mechanisms involving NF-κB pathway inhibition.

## Key findings

- Xuebijing reduces leukocyte infiltration and islet damage in an IBMIR model.
- Xuebijing protects islets from apoptosis and preserves function in inflammatory conditions.
- Xuebijing improves long-term outcomes in syngeneic islet transplantation.

## Abstract

Instant blood-mediated inflammatory reaction (IBMIR) is a major obstacle in clinical islet transplantation, leading to islet apoptosis and dysfunction due to inflammatory reaction. Xuebijing (XBJ), a traditional Chinese medicine, has been extensively used in the treatment of systemic inflammatory conditions and achieved remarkable effect. Giving these properties, XBJ holds promise in improving the outcomes of intrahepatic islet transplantation through inhibiting IBMIR.

The xenogeneic islet transplantation model was employed to evaluate the inhibitory effects of XBJ on IBMIR, while the syngeneic transplantation model was used to confirm that XBJ improves the long-term outcomes of intrahepatic islet transplantation through IBMIR suppression. In addition, studies were conducted under inflammatory conditions to demonstrate the protective effects of XBJ on islets in vitro, specifically its ability to preserve islet viability and function in an inflammatory environment.

In vivo IBMIR model, XBJ significantly inhibited leukocyte infiltration, leading to reduced islet damage. In vitro, XBJ provided direct protection to islets in inflammatory stimulation, preventing apoptosis and preserving islet function. These protective effects were further demonstrated in the syngeneic islet transplantation model, where XBJ markedly improved the outcomes of intrahepatic islet transplantation.

This study provides the evidence that XBJ improves islet transplantation outcomes through dual mechanisms targeting the IBMIR. As an already approved drug, XBJ presents a promising and readily translatable adjunctive therapy for clinical intrahepatic islet transplantation.

## Full-text entities

- **Genes:** NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}
- **Diseases:** inflammatory (MESH:D007249)

## Full text

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## Figures

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## References

48 references — full list in the complete paper: https://tomesphere.com/paper/PMC12771108/full.md

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Source: https://tomesphere.com/paper/PMC12771108