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1.
Key Laboratory of Tropical Biological Resources of the Ministry of Education and One Health Institute, School of Pharmaceutical Sciences, Hainan University, Haikou 570228, China; School of Life Science and Technology, China Pharmaceutical University, Nanjing 211198, China.
Authors
Si ZL
1
(1 author)
2.
Key Laboratory of Tropical Biological Resources of the Ministry of Education and One Health Institute, School of Pharmaceutical Sciences, Hainan University, Haikou 570228, China; State Key Laboratory of Natural Medicines, Department of TCM Pharmaceuticals, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China.
Authors
Wang HY
2
Cao YZ
2
Li QZ
2
Huang Z
2
Zhang ZH
2
(5 authors)
3.
State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, P.R. China.
Authors
Wang T
3
Liu HW
3
(2 authors)
4.
Department of Nephrology, Jiangsu Province Hospital (The First Affiliated Hospital of Nanjing Medical University), Nanjing 210029, China.
Authors
Liu K
4
(1 author)
5.
Key Laboratory of Tropical Biological Resources of the Ministry of Education and One Health Institute, School of Pharmaceutical Sciences, Hainan University, Haikou 570228, China.
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Abstract
Renal fibrosis, inflammation, and gut dysbiosis are all linked to chronic kidney disease (CKD). Here we show that Bacteroides ovatus protects against renal fibrosis. Mechanistically, B. ovatus enhances intestinal hyodeoxycholic acid (HDCA) levels by upregulating a strain of intestinal bacteria, Clostridium scindens, that has the capacity for direct HDCA production in mice. HDCA significantly promoted GLP-1 secretion by upregulating the expression of TGR5 and downregulating the expression of farnesoid X receptor (FXR) in the gut. Activation of renal GLP-1R attenuates renal fibrosis while delaying the subsequent development of CKD. In addition, HDCA can also protect against renal fibrosis by directly upregulating renal TGR5. The natural product neohesperidin (NHP) was found to exert its anti-renal fibrotic effects by promoting the growth of B. ovatus. Our findings provide mechanistic insights into the therapeutic potential of B. ovatus, C. scindens, and HDCA in treating CKD.
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