Yin-Ping Guo1,2,3, Li Shao4, Li Wang1,2,3, Man-Yun Chen1,2,3, Wei Zhang1,2,3, Wei-Hua Huang5,6,7,8. 1. Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China. 2. Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China. 3. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Xiangya Road 110, 410008, Changsha, China. 4. Department of Pharmacognosy, School of Pharmacy, Hunan University of Chinese Medicine, Changsha, 410128, Hunan, China. 5. Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China. endeavor34852@csu.edu.cn. 6. Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China. endeavor34852@csu.edu.cn. 7. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Xiangya Road 110, 410008, Changsha, China. endeavor34852@csu.edu.cn. 8. NHC Key Laboratory of Birth Defect for Research and Prevention (Hunan Provincial Maternal and Child Health Care Hospital), Changsha, 410008, Hunan, China. endeavor34852@csu.edu.cn.
Abstract
BACKGROUND: Ginsenoside CK (GCK) serves as the potential anti-colorectal cancer (CRC) protopanaxadiol (PPD)-type saponin, which could be mainly bio-converted to yield PPD by gut microbiota. Meanwhile, the anti-CRC effects of GCK could be altered by gut microbiota due to their different diversity in CRC patients. We aimed to investigate the bioconversion variation of GCK mediated by gut microbiota from CRC patients by comparing with healthy subjects. METHODS: Gut microbiota profiled by 16S rRNA gene sequencing were collected from healthy volunteers and CRC patients. GCK was incubated with gut microbiota in vitro. A LC-MS/MS method was validated to quantify GCK and PPD after incubation at different time points. RESULTS: The bioconversion of GCK in healthy subjects group was much faster than CRC group, as well as the yield of PPD. Moreover, significant differences of PPD concentration between healthy subjects group and CRC group could be observed at 12 h, 48 h and 72 h check points. According to 16S rRNA sequencing, the profiles of gut microbiota derived from healthy volunteers and CRC patients significantly varied, in which 12 differentially abundant taxon were found, such as Bifidobacterium, Roseburia, Bacteroides and Collinsella. Spearman's correlation analysis showed bacteria enriched in healthy subjects group were positively associated with the biotransformation of GCK, while bacteria enriched in CRC group displayed non correlation character. Among them, Roseburia which could secrete β-glycosidase showed the strongest positive association with the bioconversion of GCK. CONCLUSIONS: The bioconversion of GCK in healthy subjects was much faster than CRC patients mediated by gut microbiota, which might alter the anti-CRC effects of GCK.
BACKGROUND:GinsenosideCK (GCK) serves as the potential anti-colorectal cancer (CRC) protopanaxadiol (PPD)-type saponin, which could be mainly bio-converted to yield PPD by gut microbiota. Meanwhile, the anti-CRC effects of GCK could be altered by gut microbiota due to their different diversity in CRCpatients. We aimed to investigate the bioconversion variation of GCK mediated by gut microbiota from CRCpatients by comparing with healthy subjects. METHODS: Gut microbiota profiled by 16S rRNA gene sequencing were collected from healthy volunteers and CRCpatients. GCK was incubated with gut microbiota in vitro. A LC-MS/MS method was validated to quantify GCK and PPD after incubation at different time points. RESULTS: The bioconversion of GCK in healthy subjects group was much faster than CRC group, as well as the yield of PPD. Moreover, significant differences of PPD concentration between healthy subjects group and CRC group could be observed at 12 h, 48 h and 72 h check points. According to 16S rRNA sequencing, the profiles of gut microbiota derived from healthy volunteers and CRCpatients significantly varied, in which 12 differentially abundant taxon were found, such as Bifidobacterium, Roseburia, Bacteroides and Collinsella. Spearman's correlation analysis showed bacteria enriched in healthy subjects group were positively associated with the biotransformation of GCK, while bacteria enriched in CRC group displayed non correlation character. Among them, Roseburia which could secrete β-glycosidase showed the strongest positive association with the bioconversion of GCK. CONCLUSIONS: The bioconversion of GCK in healthy subjects was much faster than CRCpatients mediated by gut microbiota, which might alter the anti-CRC effects of GCK.
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