INTRODUCTION: Dysfunction of the endothelium contributes to pathological conditions of the arterial wall including atherosclerosis as a result of immunological and/or inflammatory responses. Salvianolic acid B (Sal B), a pure and active compound extracted from the Chinese herb Salvia miltiorrhizae (SM) was characterized for its anti-inflammatory and anti-oxidant properties on vascular system. METHODS AND RESULTS: Sal B pretreatment significantly inhibited the IFN-γ-induced phosphorylations of JAK2 (Tyr 1007/1008) and STAT1 (Tyr701 and Ser727). Consistently, IFN-γ-induced STAT1 downstream targets CXC chemokines' IP-10, Mig, and I-TAC were suppressed by Sal B pretreatment. Sal B inhibited promoter activities of IP-10 and the secretion of IP-10 protein. The monocyte adhesion to IFN-γ-treated ECs was observed to be reduced after Sal B pretreatment. ECs treated with Sal B alone also increased the expression of PIAS1 and SOCS1 which may also contribute to its inhibitory effect on JAK-STAT1 signaling pathways. CONCLUSIONS: The anti-inflammatory properties of Sal B on IFN-γ-induced JAK-STAT1 activation were demonstrated in the present study which provides a molecular basis for possible therapeutic usage on vascular disorders.
INTRODUCTION: Dysfunction of the endothelium contributes to pathological conditions of the arterial wall including atherosclerosis as a result of immunological and/or inflammatory responses. Salvianolic acid B (Sal B), a pure and active compound extracted from the Chinese herb Salvia miltiorrhizae (SM) was characterized for its anti-inflammatory and anti-oxidant properties on vascular system. METHODS AND RESULTS:Sal B pretreatment significantly inhibited the IFN-γ-induced phosphorylations of JAK2 (Tyr 1007/1008) and STAT1 (Tyr701 and Ser727). Consistently, IFN-γ-induced STAT1 downstream targets CXC chemokines' IP-10, Mig, and I-TAC were suppressed by Sal B pretreatment. Sal B inhibited promoter activities of IP-10 and the secretion of IP-10 protein. The monocyte adhesion to IFN-γ-treated ECs was observed to be reduced after Sal B pretreatment. ECs treated with Sal B alone also increased the expression of PIAS1 and SOCS1 which may also contribute to its inhibitory effect on JAK-STAT1 signaling pathways. CONCLUSIONS: The anti-inflammatory properties of Sal B on IFN-γ-induced JAK-STAT1 activation were demonstrated in the present study which provides a molecular basis for possible therapeutic usage on vascular disorders.
Authors: Qing Liu; Jianping Li; Adam Hartstone-Rose; Jing Wang; Jiqiang Li; Joseph S Janicki; Daping Fan Journal: Evid Based Complement Alternat Med Date: 2015-05-18 Impact factor: 2.629