Xu Yan, Feng Dechun, Wang Ying, Lin Shuting, Xu Lingyun
Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, People's Republic of China.
J Clin Immunol. 2008 Sep;28(5):512-9. doi: 10.1007/s10875-008-9206-3. Epub 2008 May 24.
Sodium tanshinone IIA sulfonate (STS) is a water-soluble derivative of tanshinone IIA, the main pharmacologically active component of Salvia miltiorrhiza. The aim of this study was to investigate the effect of STS on concanavalin A (ConA)-induced hepatitis (CIH) in mice, an experimental model of immune-mediated liver injury.
C57BL/6 mice pretreated with STS released much less alanine transaminase into plasma in response to ConA challenge and had reduced inflammatory infiltration and hepatocyte apoptosis in the liver compared with control mice pretreated with vehicle solutions. Thus, STS protected mice from CIH. In STS-pretreated mice induced with CIH, we found abrogated tumor necrosis factor-alpha and interferon (IFN)-gamma production. Moreover, mRNA expressions of IFN-inducible protein-10 and macrophage inflammatory protein-1alpha in these mice were decreased. The mechanism of anti-inflammatory effects of STS may be attributed to its modulation of crucial inflammatory signaling pathways, including NF-kappaB and IFN-gamma/STAT1.
In conclusion, STS was capable of protecting mice from immune-mediated liver injury in vivo, and the protection was associated with its suppressive effect on the production of important inflammatory mediators through modulating NF-kappaB and IFN-gamma/STAT1 signaling pathways.
丹参酮IIA磺酸钠（STS）是丹参主要药理活性成分丹参酮IIA的水溶性衍生物。本研究旨在探讨STS对刀豆蛋白A（ConA）诱导的小鼠肝炎（CIH）的影响，CIH是一种免疫介导性肝损伤的实验模型。
与用赋形剂溶液预处理的对照小鼠相比，用STS预处理的C57BL/6小鼠在ConA攻击后向血浆中释放的丙氨酸转氨酶少得多，并且肝脏中的炎症浸润和肝细胞凋亡减少。因此，STS保护小鼠免受CIH的影响。在用CIH诱导的STS预处理小鼠中，我们发现肿瘤坏死因子-α和干扰素（IFN）-γ的产生被消除。此外，这些小鼠中IFN诱导蛋白-10和巨噬细胞炎性蛋白-1α的mRNA表达降低。STS抗炎作用的机制可能归因于其对关键炎症信号通路的调节，包括NF-κB和IFN-γ/STAT1。
总之，STS能够在体内保护小鼠免受免疫介导的肝损伤，并且这种保护与其通过调节NF-κB和IFN-γ/STAT1信号通路对重要炎症介质产生的抑制作用有关。
