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Updated: Jul 14, 2026
Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
Compound Kushen injection improves M1 macrophage polarisation and radiation-induced colitis by regulating
Xin Sun1, Zheng Li2, Shangfei Luo1
1Innovation Research Institute of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, 4655 Daxue Road Changqing District, Ji'nan, Shandong 250355, China.
Background:
Radiation-induced colitis (RIC) is a common complication following radiotherapy for pelvic and abdominal malignancies. Dysregulated polarisation of macrophages towards the pro-inflammatory classically activated M1 phenotype is a key driver of RIC progression.
Purpose:
This study sought to examine the protective influence of compound Kushen injection (CKI) against RIC and clarify the mechanisms underlying these protective effects.
Methods And Results:
Mice were subjected to whole-abdominal irradiation (14 Gy) to model the clinical characteristics of RIC. The mice in the treatment groups received intraperitoneal injections of different doses of CKI for 3 days before exposure to ionising radiation (IR) and were euthanised 7 days after IR. CKI significantly increased the survival rate, body weight, and colon length of IR mice, and it ameliorated the IR-induced tissue damage, intestinal barrier disruption, elevated inflammatory factor levels, macrophage infiltration, and M1 polarisation. Mechanistically, CKI markedly suppressed Piezo1 activation and expression in macrophages as well as the Piezo1-mediated activation of the nuclear factor kappa B (NF-κB) and the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome. Notably, macrophage-specific Piezo1 ablation significantly attenuated the therapeutic efficacy of CKI through impaired mechanosensing, while concomitantly diminishing the magnitude of M1 polarisation and blunting NF-κB/NLRP3 signalling transduction.
Conclusion:
In conclusion, our findings demonstrated that CKI can improve RIC by modulating the Piezo1-mediated NF-κB/NLRP3 pathway and macrophage polarisation, thereby identifying a potential therapeutic target for RIC management and pharmacological intervention.
Insights
Compound Kushen injection (CKI) protects against radiation-induced colitis (RIC) by suppressing Piezo1 activation in macrophages. This modulation of the Piezo1-NF-κB/NLRP3 pathway reduces inflammation and improves outcomes in RIC.
Area of Science:
- Gastroenterology
- Immunology
- Radiotherapy Research
Background:
- Radiation-induced colitis (RIC) is a frequent consequence of pelvic radiotherapy.
- Macrophage polarization to the M1 phenotype drives RIC progression.
Purpose of the Study:
- To investigate the protective effects of compound Kushen injection (CKI) on RIC.
- To elucidate the underlying mechanisms of CKI's therapeutic action.
Main Methods:
- A mouse model of RIC was established using whole-abdominal irradiation (14 Gy).
- Mice received CKI intraperitoneally before irradiation.
- Macrophage activation, Piezo1 expression, NF-κB, and NLRP3 inflammasome signaling were analyzed.
Main Results:
- CKI significantly improved survival rates, body weight, and colon length in RIC mice.
- CKI ameliorated tissue damage, intestinal barrier dysfunction, and inflammatory markers.
- CKI suppressed macrophage Piezo1 activation and the subsequent NF-κB/NLRP3 inflammasome pathway.
Conclusions:
- CKI demonstrates protective effects against RIC.
- CKI functions by modulating macrophage polarization via the Piezo1-NF-κB/NLRP3 pathway.
- CKI represents a potential therapeutic strategy for managing RIC.
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