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Protosappanin A (PTA), an immunosuppressive ingredient and major biphenyl compound isolated from Caesalpinia sappan L, suppresses JAK2/STAT3-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3[1]. JAK2 STAT3

Protosappanin A (PTA: 12.5, 25, 50 μM, 24 hours) significantly inhibits the production of TNF-α and IL-1β in LPS-activated BV2 microglia. And the mRNA expressions of IL-6, IL-1β, and MCP-1 are reduced by PTA in a dose-dependent manner in BV2 microglial cell line[1].Protosappanin A (PTA: 12.5, 25, 50 μM, 24 hours) suppresses JAK2/STAT3-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3, as well as STAT3 nuclear translocation against LPS treatment[1].Protosappanin A (PTA: 12.5, 25, 50 μM, 24 hours) shows obvious effect on disturbing the interaction of transmembrane protein CD14 with Toll-like receptor-4, resulting in the inhibition of NF-κB-dependent oxidative and nitrative stress in LPS-induced BV2 microglia[2]. Western Blot Analysis[1] Cell Line: Murine BV2 microglial cell line.

[1]. Wang LC, et al. Protosappanin A exerts anti-neuroinflammatory effect by inhibiting JAK2-STAT3 pathway in lipopolysaccharide-induced BV2 microglia. Chin J Nat Med. 2017 Sep;15(9):674-679. [2]. Zeng KW, et al. Protosappanin A inhibits oxidative and nitrative stress via interfering the interaction of transmembrane protein CD14 with Toll-like receptor-4 in lipopolysaccharide-induced BV-2 microglia. Int Immunopharmacol, 2012, 14(4): 558- 569.

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