3 years ago

Fecal metabolomic dataset of American ginseng-treated DSS mice: Correlation between ginseng enteric inflammation inhibition and its biological signatures

Chong-zhi Wang, Chun-feng Zhang, Qi-hui Zhang, Julia Hesse-fong, Mallory Lager, Wei Du, Ming Xu, Chun-su Yuan

Publication date: December 2018

Source: Data in Brief, Volume 21

Author(s): Chong-Zhi Wang, Chun-Feng Zhang, Qi-Hui Zhang, Julia Hesse-Fong, Mallory Lager, Wei Du, Ming Xu, Chun-Su Yuan

Abstract

Although anti-inflammatory effects of American ginseng metabolites have been investigated at systemic and cellular levels, the biological signatures of ginseng microbial metabolite-induced bioactivities are still unknown. To fill this knowledge gap and to support the findings published in the companion research article entitled “American ginseng microbial metabolites attenuated DSS-induced colitis and abdominal pain” (Wang et al., 2018), we are here to provide datasets of enteric microbiome biotransformation and fecal metabolomics. For the microbiome biotransformation study, data were obtained from C57BL6 mice treated with a broad-spectrum antibiotic metronidazole. After oral administration of ginseng extract, we observed that compound K (CK) was undetectable in metronidazole-treated mouse stools but was detected in stools from vehicle-treated mice, suggesting biotransformation of CK is gut microbial dependent. In the fecal metabolomic study, three small molecules which were associated with gut inflammation were identified. In the DSS mice, the levels of lactate, linoleic acid, and malic acid increased significantly in the model group. After ginseng treatment, the expressions of these metabolites reduced significantly. Thus, the selective fecal endogenous metabolites could be used as biological signatures reflecting severity of enteric inflammation and ginseng treatment outcomes. Our results showed the enteric microbiome plays a key role for CK conversion, and the effects of CK on enteric inflammation can be demonstrated by the metabolomics data.

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