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Daikenchuto ameliorates muscle hypercontractility in a murine T-cell-mediated persistent gut motor dysfunction model
Hirotada Akiho1, Kazuhiko Nakamura
1Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan. akiho@intmed3.med.kyushu-u.ac.jp
Digestion
|January 27, 2011
Summary
Daikenchuto (DKT) reduced intestinal hypercontractility and modulated cytokine expression after inflammation in mice. This suggests DKT may offer new treatments for gut motor dysfunction disorders.
Area of Science:
- Gastroenterology
- Immunology
- Pharmacology
Background:
- Functional gastrointestinal disorders like IBS involve low-grade inflammation and immune changes.
- Acute inflammation induced by anti-CD3 antibody (αCD3) causes persistent intestinal smooth muscle hypercontractility.
Purpose of the Study:
- To investigate the effects of daikenchuto (DKT) on αCD3-induced intestinal smooth muscle hypercontractility.
- To analyze DKT's impact on cytokine expression following acute inflammation.
Main Methods:
- BALB/c mice were injected with αCD3 and treated with DKT.
- Intestinal muscle strip and cell contractility were measured.
- Gene and protein expression of cytokines were analyzed using real-time PCR and multiplex immunoassays.
Main Results:
- αCD3 injection significantly increased intestinal muscle hypercontractility.
- DKT treatment ameliorated this αCD3-induced hypercontractility.
- DKT significantly decreased protein levels of IL-13 and IL-17, despite moderate effects on mRNA.
Conclusions:
- Intestinal muscle contractility changes persist after inflammation resolution in a T-cell-mediated model.
- DKT modulates cytokine expression and function.
- DKT shows potential for developing new pharmacotherapeutic strategies for gut motor dysfunction.
