Planta Med 2019; 85(18): 1538
DOI: 10.1055/s-0039-3400060
Main Congress Poster
Poster Session 2
© Georg Thieme Verlag KG Stuttgart · New York

Mechanism for anti-inflammatory effects of Farnesiferol B in ischemia/reperfusion injury of kidney

L Zhang
1   Department of Clinical Pharmacology and Toxicology, University Hospital Zurich,, 8006 Zurich, Switzerland
2   College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine,, 250355, Jinan China
,
X Fu
3   Key Laboratory of Traditional Chinese Medicine for Classical Theory, Ministry of Education, Shandong University of Traditional Chinese Medicine,, 250355, Jinan China
4   Institute for Literature and Culture of Chinese Medicine, Shandong University of Traditional Chinese Medicine,, 250355 Jinan, China
,
T Wang
4   Institute for Literature and Culture of Chinese Medicine, Shandong University of Traditional Chinese Medicine,, 250355 Jinan, China
,
Z Wang
4   Institute for Literature and Culture of Chinese Medicine, Shandong University of Traditional Chinese Medicine,, 250355 Jinan, China
,
Z Gai
1   Department of Clinical Pharmacology and Toxicology, University Hospital Zurich,, 8006 Zurich, Switzerland
3   Key Laboratory of Traditional Chinese Medicine for Classical Theory, Ministry of Education, Shandong University of Traditional Chinese Medicine,, 250355, Jinan China
,
GA Kullak-Ublick
1   Department of Clinical Pharmacology and Toxicology, University Hospital Zurich,, 8006 Zurich, Switzerland
5   Mechanistic Safety, CMO & Patient Safety, Global Drug Development, Novartis Pharma,, 4056 Basel, Switzerland
› Author Affiliations
Further Information

Publication History

Publication Date:
20 December 2019 (online)

 

Inflammation plays an important role in the pathophysiological progression of ischemia/reperfusion (I/R)-induced kidney injury. TGR5 regulates macrophage reactivity and attenuates inflammation in different disease models. We aimed to investigate the effects and mechaism on Farnesiferol B as a TGR5 agonist in renal I/R injury. Results showed that Farnesiferol B-treated mice reduced the tubular injury score by 47%. Farnesiferol B reduced renal oxidative stress by H2O2 and NGAL (23% and 218% respectively) and significantly decreased inflammation factors TNF-a (31%) and MCP-1 ( 52%) compared with I/R groups. Gene expression of IL-6 and Icam was reduced to 0.64 and 0.37 fold of those of I/R groups. In vitro, Farnesiferol B treatment alleviated LPS-induced macrophage migration and NF-κB activation through TGR5. In conclusion, Farnesiferol B could protect kidney function from I/R-induced damage by attenuating inflammation reaction though activating TGR5 in macrophage. This might be a potent TGR5 ligand for the treatment against I/R-induced renal inflammation.