Title : Urolithin A targets the PI3K/Akt/NF-κB pathways and prevents IL-1β-induced inflammatory response in human osteoarthritis: in vitro and in vivo studies.

Pub. Date : 2019 Sep 1

PMID : 31497826






4 Functional Relationships(s)
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1 In vitro, UA inhibited the interleukin-1 beta (IL-1beta) induced over-production of nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in a concentration-dependent manner in human OA chondrocytes. Dinoprostone interleukin 1 beta Homo sapiens
2 In vitro, UA inhibited the interleukin-1 beta (IL-1beta) induced over-production of nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in a concentration-dependent manner in human OA chondrocytes. Dinoprostone interleukin 1 beta Homo sapiens
3 In vitro, UA inhibited the interleukin-1 beta (IL-1beta) induced over-production of nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in a concentration-dependent manner in human OA chondrocytes. Dinoprostone interleukin 1 beta Homo sapiens
4 In vitro, UA inhibited the interleukin-1 beta (IL-1beta) induced over-production of nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in a concentration-dependent manner in human OA chondrocytes. Dinoprostone interleukin 1 beta Homo sapiens