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Nuclear magnetic resonance-based metabolomics approach to evaluate the prevention effect of Camellia nitidissima Chi on colitis-associated carcinogenesis

ABSTRACT: Colorectal cancer (CRC) is one of the most common malignant tumors worldwide, occurring in the colon or rectum portion of large intestine. With marked antioxidant, anti-inflammation and anti- tumor activities, Camellia nitidissima Chi has been used as an effective treatment of cancer. The azoxymethane/dextran sodium sulfate (AOM/DSS) induced CRC mice model was established and the prevention effect of Camellia nitidissima Chi extracts on the evolving of CRC was evaluated by gross examination, histopathological inspection, serum biochemistry analysis, combined with nuclear magnetic resonance (NMR)-based metabolomics and correlation network analysis. The results showed that Camellia nitidissima Chi extracts could significantly inhibit AOM/DSS induced CRC, relieve the colonic pathology and ameliorate the serum biochemistry, and could signiﬁcantly reverse the disturbed metabolism towards the normal state. Moreover, the butanol fraction showed a better efficiency than the water-soluble fraction of Camellia nitidissima Chi. The study pave the way for further development of Camellia nitidissima Chi extracts as a potent CRC inhibitor. In this work, rats were divided into control group, carcinoma group, and two drug groups of JHC and CNC. The acronyms JHC means the water-soluble fraction of Camellia nitidissima Chi. The acronyms CNC means the butanol fraction of Camellia nitidissima Chi.

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Spleen, Intestine, Kidney

DISEASE(S): Cancer

SUBMITTER: Minghui Li

PROVIDER: ST000782 | MetabolomicsWorkbench | Sun May 21 00:00:00 BST 2017

REPOSITORIES: MetabolomicsWorkbench

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Project description:Nonresolving inflammation is correlated to carcinogenesis. Ulcerative colitis-associated colorectal cancer (UC-CRC), one of the typical carcinoma generated by inflammation that cannot be resolved properly, has been widely believed to involve a multistep process contains M-bM-^@M-^\inflammation-dysplasia-cancerM-bM-^@M-^] sequence. The exact molecular mechanisms underlying the step-wise development of UC-CRC is still not fully understood. Detecting the changes in gene expression profiles may help to reveal why and how does the prolonged inflammatory response lead to carcinogenesis, and to characterize potential diagnostic/prognostic markers or additional therapeutic targets for UC-CRC. There for, we performed temporal genome expression profiling analysis using the Affymetrix genome wide microarray system to identify broad scale changes in gene expression associated with the development of colitis-associated cancer, based on an AOM/DSS induced mouse model of UC-CRC. 6-week-old male ICR mice were given a single intraperitoneal injection of AOM (10mg/kg) at Day 1, followed by three cycles of DSS administration (cycle 1: 2%, Day 8~14; cycle 2: 1.5%, Day 29~33; cycle 3: 1.5%, Day 50~54) in the drinking water. Instead, control group of mice were given a single intraperitoneal injection of saline (10mg/kg) at Day 1 and distilled water drinking from the beginning to the end without DSS. Colorectal tissues were collected at days 14, 28, 42, 56 and 140 (at the end of the 2nd, 4th, 6th, 8th and 20th week) from the AOM/DSS group and at day 14 from the control group. Pathological changes of each sample were identified under microscope. Samples collected at the end of the 2nd week were inflamed mucosae, the 4th week were low grade dysplasias, the 6th week were high grade dysplasias, the 8th week were high grade dysplasias with active inflammation, the 20th week were carcinomas, and the control sample were normal mucosae. Total RNA were extracted and detected by Affymerix GeneChip Mouse Genome 430 2.0 Array.

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Nuclear magnetic resonance-based metabolomics approach to evaluate the prevention effect of Camellia nitidissima Chi on colitis-associated carcinogenesis

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