中文摘要：

目的观察氯化钆（GdCl3）对大鼠腹腔巨噬细胞（PMΦ）表达CD68是否有抑制作用。方法取正常大鼠PM中体外培养，用不同浓度的GdCl3处理PM中；采用弗氏完全佐剂（FCA）诱导大鼠佐剂性关节炎（AA）模型并尾静脉注射GdCl3。采用免疫荧光双标、Westernblot法检测PM西活化标记物CD68的表达情况。结果在一定的浓度范围内，GdCl3可抑制体外培养的正常大鼠PMΦ中CD68的表达，以5×10^-6mol／L浓度抑制效果最明显。大剂量的GdCl3对细胞有明显的毒性作用，表现为细胞的形态和核发生改变，并可诱导内质网（ER）应激相关蛋白ARMET的表达。对于AA大鼠活化的PMSP，体内注射GdCl3（10mg／kg）可使部分CD68阳性的PM中转阴，同时促进这些阴性细胞的分化；GdCl3并可诱导部分活化的PMCD凋亡。结论GdCl3可以抑制大鼠PMΦ中CD68的表达及诱导活化的PMSP凋亡，这可能是GdCl3抑制PM中活化的机制之一。

英文摘要：

Objective To investigate whether gadolinium chloride inhibits the expression of CD68 in rat peritoneal macrophages （PMΦs）. Methods PMΦs were isolated from normal SD rats and treated with different concentrations of gadolinium chloride （ GdCl3 ）. Rat adjuvant arthritis （AA） was induced by Freund＇s complete adjuvant （FCA）. PMΦs were harvested after injection of GdCl3 through tail vein. Double immunofluoreseence labeling and western blotting were used to determine the expression of CD68. The nuclus were stained by DAPI. TUNEL staining was used to determine the apoptotic PMΦs. Results GdCl3 dose-dependently inhibited the expression of CD68 in PMΦs from normal rats. The optimal concentration was 5 × 10^-6 mol/L. The higher concentrations of GdCl3 were toxic to PMΦs, including the changes in cellular morphologies and nuclus. Furthermore, it up-regulated the expression of ARMET, a secreting protein inducible to ER stress at the higher concentrations. GdCl3 also turn some of the CD68- positive PMΦs of AA rats to negative ones and promoted these negative PMΦs differentiation at the dose of 10 mg/ kg. Meanwhile, GdCl3 induced some of the activated PMΦs apoptosis. Conclusion GdCl3 inhibits the expression of CD68 both in normal and activated PMΦs and induces PMdPs apoptosis, which probably is one of the mechanisms that contribute to the inhibition of PMΦ activation.