Acute graft-versus-host disease (aGvHD) remains lethal, even after allogeneic hematopoietic stem cell transplantation. Inflammatory responses play an important role in aGvHD. Salvianolic acid B (Sal B) has been widely reported to have a major effect on the anti-inflammatory response, but these effects in an aGvHD model have never been reported. B6 donor splenocytes were transplanted into unirradiated BDF1 recipients and liver and serum were collected on day 14 after transplantation with or without Sal B administration. We measured the expression of pro-inflammatory cytokines and chemokines and other manifestations in aGvHD mice after Sal B treatment. Sal B ameliorated liver injury in aGvHD and promoted survival in mice. Sal B treatment resulted in decreased expression of pro-inflammatory cytokines and chemokines whose expressions in liver are normally elevated by aGvHD. Furthermore, Sal B treatment also enhanced PGC-1α expression in liver tissue and HO-1 expression in nonparenchymal cells. In addition, HO-1 inhibitor abrogated the improvement of survival rate of mice with aGvHD. These results indicated that the protective effect of Sal B relies on suppressing the inflammatory response phase in the aGvHD model, presumably by inducing HO-1. Taken together our data showed that Sal B ameliorates liver injury in aGvHD by decreasing inflammatory responses via upregulation of HO-1. It may provide a novel way to deal with this disease.

即使同种异体造血干细胞移植后，急性移植物抗宿主病（aGvHD）仍然具有致命性。炎症反应在aGvHD中起重要作用。丹酚酸B（Sal B）已被广泛报道对抗炎反应具有重要作用，但尚未在aGvHD模型中报道这些作用。将B6供体脾细胞移植到未经辐照的BDF1受体中，并在移植后第14天收集有无Sal B的肝脏和血清。我们测量了Sal B治疗后aGvHD小鼠中促炎性细胞因子和趋化因子的表达及其他表现。Sal B改善了aGvHD的肝损伤并促进了小鼠的存活。Sal B治疗导致促炎性细胞因子和趋化因子的表达降低，而促炎性细胞因子和趋化因子在肝脏中的表达通常通过aGvHD升高。此外，Sal B处理还增强了肝组织中PGC-1α的表达和非实质细胞中HO-1的表达。此外，HO-1抑制剂可消除aGvHD小鼠的存活率。这些结果表明，Sal B的保护作用依赖于在aGvHD模型中抑制炎症反应阶段，大概是通过诱导HO-1。汇总我们的数据表明，Sal B通过上调HO-1降低炎症反应，从而改善aGvHD的肝损伤。它可能提供一种新颖的方法来治疗这种疾病。Sal B治疗还增强了肝组织中PGC-1α的表达和非实质细胞中HO-1的表达。此外，HO-1抑制剂可消除aGvHD小鼠的存活率。这些结果表明，Sal B的保护作用依赖于在aGvHD模型中抑制炎症反应阶段，大概是通过诱导HO-1。综合我们的数据显示，Sal B通过上调HO-1降低炎症反应，从而改善aGvHD的肝损伤。它可能提供一种新颖的方法来治疗这种疾病。Sal B治疗还增强了肝组织中PGC-1α的表达和非实质细胞中HO-1的表达。此外，HO-1抑制剂可消除aGvHD小鼠的存活率。这些结果表明，Sal B的保护作用依赖于在aGvHD模型中抑制炎症反应阶段，大概是通过诱导HO-1。综合我们的数据显示，Sal B通过上调HO-1降低炎症反应，从而改善aGvHD的肝损伤。它可能提供一种新颖的方法来治疗这种疾病。综合我们的数据显示，Sal B通过上调HO-1降低炎症反应，从而改善aGvHD的肝损伤。它可能提供一种新颖的方法来治疗这种疾病。综合我们的数据显示，Sal B通过上调HO-1降低炎症反应，从而改善aGvHD的肝损伤。它可能提供一种新颖的方法来治疗这种疾病。