Abstract

sBackgroundShaoyao decoction (SYD) is a traditional Chinese medicine prescription formulated by Liu Wan-Su, a master of traditional Chinese medicine in Jin-Yuan Dynasty. SYD is effective in treating ulcerative colitis. Paeonol, a component of SYD, inhibits colorectal cancer (CRC) cell proliferation and induces CRC cell apoptosis. In this study, azoxymethane (AOM)/dextran sodium sulfate (DSS)–induced colitis-associated CRC (caCRC) model and CRC cell lines were used to examine the effects of SYD on CRC in vivo and in vitro.MethodsA translational medicine strategy based on phytomics quality control was adopted. Liquid chromatography was employed for the chemical characterization and chemical fingerprinting of SYD. Protein expression and macrophage existence were determined by immunohistochemistry and western blot. Serum cytokines were quantified by Luminex assay.ResultsAOM/DSS-induced caCRC phenotypically resembled human caCRC. SYD significantly increased the survival rate of the mice, ameliorated the general well-being of the mice, and reduced the incidence and multiplicity of colonic neoplasms. SYD inhibited epithelial–mesenchymal transition (EMT), as indicated by upregulated epithelia cadherin and downregulated neuronal cadherin, fibronectin, vimentin, and transcription factor Snail. SYD reduced the expression levels of serum interleukin 1β, interleukin-6, tumor necrosis factor α, tumor-associated macrophages, and p65. These results showed that SYD can attenuate proinflammatory cytokines and inhibit EMT.ConclusionsSYD ameliorates caCRC by suppressing inflammation and inhibiting EMT. SYD might be an alternative therapy for caCRC.

Highlights

  • 142,820 (9%) and 50,830 (9%) new cancer cases and deaths of colorectal cancer (CRC) were reported in the US in 2013, respectively [1]

  • Shaoyao decoction (SYD) reduced the expression levels of serum interleukin 1β, interleukin-6, tumor necrosis factor α, tumor-associated macrophages, and p65. These results showed that SYD can attenuate proinflammatory cytokines and inhibit epithelial–mesenchymal transition (EMT)

  • SYD might be an alternative therapy for colitis-associated CRC (caCRC)

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Summary

Introduction

142,820 (9%) and 50,830 (9%) new cancer cases and deaths of colorectal cancer (CRC) were reported in the US in 2013, respectively [1]. CRC is the third most common cancer in men and the second in women worldwide [2]. Ulcerative colitis, familial adenomatous polyposis, and hereditary nonpolyposis colon cancer syndrome are the three highest risk groups for developing CRC. In a metaanalysis based on 116 studies, the overall prevalence of colorectal cancer in patients with ulcerative colitis was 3.7%. The pathogenesis of colorectal cancer in patients with ulcerative colitis is triggered by inflammation-dependent mechanisms [4]. SYD is effective in treating ulcerative colitis. A component of SYD, inhibits colorectal cancer (CRC) cell proliferation and induces CRC cell apoptosis. Azoxymethane (AOM)/dextran sodium sulfate (DSS)–induced colitis-associated CRC (caCRC) model and CRC cell lines were used to examine the effects of SYD on CRC in vivo and in vitro

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