1. Metabolomic mechanisms for the clinical phenomes of spleen deficiency and dampness-heat syndrome and dampness-heat accumulation syndrome associated with colorectal cancer.
- Author
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TIAN Yuan, YANG Zhongming, DU Xin, HUANG Jin, YE Lingyu, Linda, and DUAN Dayue, Darrel
- Subjects
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LIQUID chromatography-mass spectrometry , *COLORECTAL cancer , *KREBS cycle , *HEAT stroke , *METABOLOMICS , *SPLEEN - Abstract
Objective To elucidate the metabolomic mechanisms for the clinical phenomes of spleen deficiency and dampness-heat syndrome (PXSR) and the dampness-heat accumulation syndrome (SRYJ) associated with colorectal cancer (CRC). Methods From March 2021 to October 2021, A total of 68 patients with spleen deficiency and dampness-heat syndrome and 58 patients with dampness-heat accumulation syndrome of colorectal cancer were recruited in the Affiliated Hospital of Traditional Chinese Medicine of Southwest Medical University, and 62 healthy control with balanced constitution personnel who underwent physical examination here. Cohorts were established for PXSR phenome (PXSRP), SRYJ phenome (SRYJP), and healthy control with balanced constitution (BC). Serum metabolites were isolated and identified by non-targeted metabolomics and ultra-high liquid chromatography and mass spectrometry (UHPLC-QE-MS) ; the results were further analyzed by principal component analysis (PCA), Orthogonal partial least squares discriminant analysis (OLPS-DA) analysis and bioinformatics analysis. Results Compared with Group BC, Group PXSRP had 12 metabolite differences, including downregulation of guanidoacetic acid, and upregulation of formiminoglat-amic acid, imidazoleacetic acid, deoxyuridine, cytidine, pseudouridine, ornithine, N-acetylornithine, 5-hydroxyindoleacetic acid, porphobilinogen, succinic acid semialdehyde, and galactitol. 7 metabolic pathways were involved, mainly involving abnormal energy metabolism. Group SRYJP had 17 metabolite differences, including upregulation of deoxyuridine, cytidine, porphobilinogen, arachidonic acid, prostaglandin B2, isocitric acid, L-gulonolactone, and downregulation of guanidoacetic acid, uridine, hydroxyproline, pyrrole-2- carboxylic acid, adenosine, 5, 6-DHET, 8, 9-DiHETrE, 9, lO-DHOME, bovinic acid, and hydroxypyruvic acid. Nine metabolic pathways were involved, mainly with lipid metabolism and tricarboxylic acid cycle abnormality. There were 4 identical characteristic metabolite differences (guanidoacetic acid, deoxyuridine, cytidine, porphobilinogen) between group PXSRP and group SRYJP. Conclusion These results reveal the metabolomic mechanism of the formation of the clinical phenomes of PXSR and SRYJ associated with CRC and provide objective metabolomic evidence for the precise diagnosis of CRC clinical phenomes. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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