Protosappanin A是从苏木中分离得到的免疫抑制成分和主要联苯化合物，通过下调JAK2和STAT3的磷酸化，抑制JAK2/STAT3依赖的炎症通路。

Protosappanin A has anti-oxidative/nitrative activities on brain immune and neuroinflammation through regulation of CD14/TLR4-dependent IKK/IIoB/NF-IoB inflammation signal pathway; it exerts anti-neuroinflammatory effect by inhibiting JAK2-STAT3 pathway in lipopolysaccharide-induced BV2 microglia. Protosappanin A induces immunosuppression of rats heart transplantation targeting T cells in grafts via NF-kappaB pathway. Protosappanin A and protosappanin B have antimicrobial activity, they show both alone activities and resistance reversal effects of amikacin and gentamicin against MRSA. Protosappanin A shows strong effect against HIV-1 IN with an IC50 value of 12.6 uM.

Protosappanin A (PsA) and Protosappanin B (PsB) were identified from Sappan Lignum extracts. They showed activity against both S. aureus and MRSA with MIC or MIC50 at 64 (PsA) and 128 (PsB) mg/L alone. When they were used in combination with antibiotics, they showed the best synergy with amikacin and gentamicin with MIC50 (mg/L) of amikacin reduced more significantly from 32 to four (with PsA) and eight (with PsB), and the fractional inhibitory concentration index (FICI) ranged between 0.078 and 0.500 (FICI50 = 0.375). Moreover, the resistance of MRSA towards amikacin and gentamicin could be reversed by the Clinical and Laboratory Standards Institute criteria. The combined bactericidal mode could as well be synergy. PsA and PsB showed very low cytotoxicity in comparison with their promising activity against MRSA[1].

102036-28-2

C15H12O5

272.25

原苏木素A;PTA

DMSO:225 mg/mL (826.45 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years