摘要
目的观察六味地黄丸对四氯化碳(CCl4)小鼠肝纤维化过程中巨噬细胞激活的影响。方法每周3次腹腔注射CCl_4共6周制备肝纤维化模型,六味地黄丸在CCl_4造模同时灌胃给药。免疫荧光检测α-SMA表达,免疫组化检测巨噬细胞标志物CD68表达,qPCR检测α-SMA、TNF-α、IL-1β、MCP1、CXCR3表达,Western blot检测α-SMA、MCP1和CXCR3。结果造模6周,α-SMA表达显著升高(P<0.01),六味地黄丸显著抑制α-SMA表达(P<0.01);CCl_4造模后CD68主要分布在纤维间隔呈强阳性表达;与正常组相比,模型组TNF-α、IL-1β、MCP1、CXCR3表达显著升高(P<0.01);与模型组相比,六味地黄丸显著降低CD68及促炎症因子、趋化因子的表达(P<0.01)。结论六味地黄丸对CCl_4肝纤维化过程中的巨噬细胞激活有显著抑制作用。
OBJECTIVE To observe the inhibitory effects of Liuwei Dihuang Pills（LWDHP） on macrophages activation in CC14-induced liver fibrosis in mice. METHODS C57BL/6 mice were induced liver fibrosis by CC14 exposure and administered with LWDHP for 6 weeks simultaneously. Liver tissue was investigated by HE and Sirius red staining, α-SMA was analyzed by immunofluorescenee, qPCR and Western blot. Liver macrophages were observed by immunohistochemistry of CD68. The pro-inflammatory cytokines and chemokine such as TNF-α, IL-1β, CXCR3 and MCP1 were detected by qPCR or Western blot analysis. RESULTS After 6 weeks of CC14 administration, the expression of α-SMA significantly increased, and LWDHP po- tently inhibited the α-SMA expression. Immunohistochemistry showed that the expression of CD68 was very weak in normal group, CD68 was distributed mainly between fibrotic septa with strong positive expression in CC14 model group; Real-time quantitative PCR showed that TNF-α, IL-1β, MCP1 and CXCR3 expression significantly increased in model group compared with normal group. Compared with the model group, LWDHP significantly reduced the expression of CD68, inflammatory fac-tors and chemotactic factors. CONCLUSION LWDHP shows a potent inhibition of macrophage activation in CC14-induced liv-er fibrosis.
出处
《南京中医药大学学报》
CAS
CSCD
北大核心
2017年第1期65-68,共4页
Journal of Nanjing University of Traditional Chinese Medicine
基金
河北大学附属医院课题(2014YJ016)
关键词
肝纤维化
六味地黄丸
巨噬细胞
liver fibrosis
Liuwei Dihuang Pills
macrophage
