目的 观察氧化低密度脂蛋白（Oxidized Low-Density Lipoprotein，ox-LDL）对系膜细胞（Mesangial Cells，MCs）分泌炎症介质功能的影 响，并从细胞分子生物学水平阐明肾康灵的作用机理。方法 采用肾康灵含药血清干预增殖系膜细胞的方法，按照随机数字表法分为7组，即正常对照组：DMEM-F12培养液； ox-LDL组：DMEM-F12培养液+ox-LDL（100 μg·mL-1）；ox-LDL+趋化因子受体（CXCR6）组：DMEM-F12培养液+ox-LDL（100 μg·mL-1）+CXCR6；肾康灵低浓度组：DMEM- F12培养液+ox-LDL（100 μg·mL-1）+肾康灵低浓度含药血清；⑤肾康灵高浓度组：DMEM-F12培养液+ox-LDL（100 μg·mL-1）+肾康灵高浓度含药血清；阿托伐他汀低浓度 组：DMEM-F12培养液+ox-LDL（100 μg·mL-1）+阿托伐他汀（50 μmol·L-1）；阿托伐他汀高浓度组：DMEM-F12培养液+ox-LDL（100 μg·mL-1））+阿托伐他汀（100 μ mol·L-1）。以上各组标本培养24 h后收集各组细胞及上清液。每组实验细胞重复培养6次。分别利用ELISA法、RT- RCR 法和Western blot 法检测趋化因子配体16（CXCL16 ）、清道夫受体-B（CD36）、干扰素-γ（IFN-γ）、白细胞介素-6（IL- 6）、肿瘤坏死因子-α（TNF-α）基因水平和蛋白含量。结果 利用ox-LDL（100 μg·mL-1））诱 导大鼠系膜细胞增殖并加入CXCR6受体后，CXCL16、CD36、IFN-γ、IL6、TNF-α的基因表达均显著升高（P＜ 0.01），肾康灵含药血清呈浓度依赖性降低其表达水平，肾康 灵高浓度组降低最显著（P＜ 0.01）。结论 ox-LDL诱导系膜细胞增殖时通过CXCR6介导，可促进CXCL16、CD36、IFN-γ、IL6、TNF-α等炎症介质的释放，肾康灵可通过抑 制炎症介质的释放，保护系膜细胞的功能。

Objective To observe the effect of oxidized low density lipoprotein（ox-LDL） on the secretion of inflammatory cytokines in mesangial cells（MCs） and to clarify the therapeutic mechanism of Shenkangling at the level of cellular molecular biology. Methods Shenkangling- containing serum（SCS） was obtained from Sprague-Dawley rats which were administered Shenkangling. DMEM-F12 culture fluid was used as the basic medium for the culture of MCs（normal control group），and then according to the grouping，100 μg/mL of ox-LDL，100 μg/mL of ox-LDL+ CXCR6，100 μg/mL of ox-LDL+low-dose SCS，100 μg/mL of ox-LDL+high-dose SCS，100 μg/mL of ox-LDL+atorvastatin 50 μmol/L，100 μg/mL of ox-LDL+atorvastatin 100 μmol/L were added separately，namely ox-LDL group，CXCR6 group，low-dose SCS group，high-dose SCS group，low-dose atorvastatin group，and high-dose atorvastatin group. After culturing for 24h，the MCs and MCs supernatant were collected. The cell culture repeated for 6 times. Expression levels of CXCL16，CD36，IFN-γ，IL-6，TNF-α mRNA and protein in MCs were detected by RT-PCR and Western blotting，respectively. Results CXCL16，CD36，IFN-γ， IL-6 and TNF-α mRNA expression levels were increased obviously in CXCR6 group，and SCS could counteract the expression levels in a dose-dependent manner（P＜ 0.05）. Conclusion ox-LDL may promote the release of inflammatory mediators of CXCL16，CD36，IFN-γ，IL-6，and TNF-α in mesangial cells mediated by CXCR6，and Shenkangling has protective effect for the function of MCs through inhibiting the release of inflammatory cytokines.

R285.5

国家自然科学基金青年基金项目（81202835）；福建省自然科学基金面上项目（2011J01199）；福建省卫生厅青年基金项目（2012-1-30）。