Related Experiment Video
Updated: Apr 16, 2026
A Mice Model of Chlorhexidine Gluconate-Induced Peritoneal Damage
Published on: April 28, 2022
The kampo medicine Daikenchuto inhibits peritoneal fibrosis in mice
Mineaki Kitamura1, Tomoya Nishino, Yoko Obata
1Second Department of Internal Medicine, Nagasaki University School of Medicine.
Abstract:
Long-term peritoneal dialysis therapy causes inflammation and histological changes in the peritoneal membrane. Inflammation generally activates fibroblasts and results in fibroblast-myofibroblast differentiation. Heat-shock protein 47 (HSP 47), a collagen-specific molecular chaperone, is localized in myofibroblasts and is involved in the progression of peritoneal fibrosis. Daikenchuto (DKT), a Kampo medicine, is used to prevent postoperative colon adhesion. It inhibits inflammation and HSP 47 expression in the gastrointestinal tract. We examined the effect of DKT on chlorhexidine gluconate (CG)-induced peritoneal fibrosis in mice injected with 0.1% CG dissolved in 15% ethanol. DKT was dissolved in the drinking water. Histological changes were assessed using Masson trichrome staining. Cells expressing α-smooth muscle actin (α-SMA), HSP 47, phospho-Smad 2/3, F4/80, and monocyte chemotactic protein-1 were examined immunohistochemically. Compared with the control group, the peritoneal tissues of the CG group were markedly thickened, and the number of cells expressing α-SMA, HSP 47, phospho-Smad 2/3, F4/80, and monocyte chemotactic protein-1 was significantly increased. However, these changes were inhibited in the DKT-treated group. These results indicate that DKT can prevent peritoneal fibrosis by inhibiting inflammation and HSP 47 expression.
Insights
Daikenchuto (DKT) prevents peritoneal fibrosis by reducing inflammation and heat-shock protein 47 (HSP 47) expression. This Kampo medicine offers a potential therapeutic strategy for dialysis-related peritoneal membrane damage.
Area of Science:
- Nephrology
- Gastroenterology
- Pharmacology
Background:
- Long-term peritoneal dialysis can cause peritoneal membrane inflammation and fibrosis.
- Fibrosis involves fibroblast activation and differentiation, with Heat-shock protein 47 (HSP 47) playing a key role.
- Daikenchuto (DKT), a Kampo medicine, is known to inhibit inflammation and HSP 47 in the gut.
Purpose of the Study:
- To investigate the efficacy of DKT in preventing chlorhexidine gluconate (CG)-induced peritoneal fibrosis in a mouse model.
- To assess DKT's impact on key markers of inflammation and fibrosis in the peritoneal membrane.
Main Methods:
- Peritoneal fibrosis was induced in mice using chlorhexidine gluconate (CG).
- DKT was administered to mice via drinking water.
- Histological changes were evaluated using Masson trichrome staining.
- Immunohistochemistry was used to quantify cells expressing α-smooth muscle actin (α-SMA), HSP 47, phospho-Smad 2/3, F4/80, and monocyte chemotactic protein-1.
Main Results:
- CG-induced peritoneal tissues showed significant thickening and increased expression of α-SMA, HSP 47, phospho-Smad 2/3, F4/80, and monocyte chemotactic protein-1 compared to controls.
- DKT treatment significantly inhibited these CG-induced changes.
- DKT effectively reduced inflammation and HSP 47 expression in the affected peritoneal tissues.
Conclusions:
- DKT demonstrates a protective effect against peritoneal fibrosis.
- DKT may prevent peritoneal fibrosis by suppressing inflammation and HSP 47 expression.
- DKT represents a potential therapeutic agent for managing peritoneal fibrosis associated with long-term dialysis.
