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DOI: 10.1055/s-0039-3400060
Mechanism for anti-inflammatory effects of Farnesiferol B in ischemia/reperfusion injury of kidney
Publikationsverlauf
Publikationsdatum:
20. Dezember 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.