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Published on: November 30, 2016
Effect of TU-100 on Colorectal Liver Metastasis in Mouse Model of Metabolic Dysfunction-Associated Steatohepatitis
Shinichiro Yamada1, Yuji Morine1, Tetsuya Ikemoto1
1Department of Digestive and Transplant Surgery, Tokushima University Hospital, Tokushima, Japan.
Introduction:
The incidence of metabolic dysfunction-associated steatohepatitis (MASH) is rapidly increasing, and colorectal liver metastasis (CLM) has been reported to be enhanced in MASH. We previously reported that the herbal medicine Daikenchuto (TU-100) regulates the intestinal microbiome and MASH in a mouse model. This study was performed to examine the effect of TU-100 on CLM using a Western diet (WD)-fed mouse model.
Methods:
Six-week-old male C57BL/6J mice were used. Mice in the WD group were fed a WD, and TU-100 was administered to mice in the WD+TU-100 group. Splenic injection of MC38 colon cancer cells was performed at 16 wk, and mice were sacrificed 2 wk after splenic injection to assess steatosis, fibrosis, and hepatic mRNA expression.
Results:
The degree of steatosis was significantly reduced in the WD+TU-100 group compared with the WD group (P < 0.05). The maximum tumor diameter was significantly smaller in the WD+TU-100 group than in the WD group (P < 0.05). Hepatic mRNA expression of serum amyloid A1 and tissue inhibitor of matrix metalloproteinases 1 was significantly suppressed in the WD+TU-100 group compared with the WD group (P < 0.05).
Conclusions:
TU-100 improved hepatic steatosis in an MASH mouse model and suppressed CLM. Suppression of hepatic serum amyloid A1 and tissue inhibitor of matrix metalloproteinases 1 expression may contribute to these effects.
