中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
CHINESE JOURNAL OF RHEUMATOLOGY
2011年
3期
151-154
,共4页
孙琳%刘湘源%赵金霞%满斯亮%张霞
孫琳%劉湘源%趙金霞%滿斯亮%張霞
손림%류상원%조금하%만사량%장하
趋化因子%关节炎,实验性%淋巴细胞
趨化因子%關節炎,實驗性%淋巴細胞
추화인자%관절염,실험성%림파세포
Chemokine%Arthritis,experimental%Lymphocytes
目的 了解CXCL16在胶原诱导性关节炎(CIA)小鼠发病中的作用.方法 以8只正常小鼠为对照,采用酶联免疫吸附试验(ELISA)和反转录-聚合酶链反应(RT-PCR)法,分别检测CXCL16在12只CIA小鼠外周血中的蛋白水平及病变滑膜组织中的mRNA水平,再采用CCK-8法、RT-PCR和ELISA,分别检测不同浓度的CXCL16重组蛋白(0,100,200,400,800 ng/ml)刺激鼠脾淋巴细胞的增殖情况、上清中白细胞介素(IL)-2和干扰素-γ水平及RANKL mRNA表达水平.采用t检验和单因素方差分析进行统计分析.结果 ①与对照组相比,CIA小鼠外周血CXCL16[分别为(72±8)和(127±10)pg/ml,P＜0.05]和滑膜CXCL16 mRNA水平(分别为0.214±0.007和0.375±0.009,P＜0.01)均显著增高.②CXCL16(200、400、800 ng/ml)作用于CIA小鼠淋巴细胞,其增殖能力明显高于CXCL16(0 ng/ml),吸光度(A)值分别为0.51±0.06、0.56±0.05、0.55±0.04、0.41±0.04(P＜0.05).并且CXCL16对CIA组小鼠淋巴细胞的增殖刺激能力明显高于其对健康对照组小鼠淋巴细胞(P均＜0.05).③核因子κB受体活化因子配体(RANKL)mRNA、IL-2和干扰素-γ水平在CIA CXCL16(400、800 ng/ml)组均明显高于CXCL16(0 ng/ml)组(P＜0.01).结论 CXCL16可能通过活化淋巴细胞在CIA发病中发挥重要作用.
目的 瞭解CXCL16在膠原誘導性關節炎(CIA)小鼠髮病中的作用.方法 以8隻正常小鼠為對照,採用酶聯免疫吸附試驗(ELISA)和反轉錄-聚閤酶鏈反應(RT-PCR)法,分彆檢測CXCL16在12隻CIA小鼠外週血中的蛋白水平及病變滑膜組織中的mRNA水平,再採用CCK-8法、RT-PCR和ELISA,分彆檢測不同濃度的CXCL16重組蛋白(0,100,200,400,800 ng/ml)刺激鼠脾淋巴細胞的增殖情況、上清中白細胞介素(IL)-2和榦擾素-γ水平及RANKL mRNA錶達水平.採用t檢驗和單因素方差分析進行統計分析.結果 ①與對照組相比,CIA小鼠外週血CXCL16[分彆為(72±8)和(127±10)pg/ml,P＜0.05]和滑膜CXCL16 mRNA水平(分彆為0.214±0.007和0.375±0.009,P＜0.01)均顯著增高.②CXCL16(200、400、800 ng/ml)作用于CIA小鼠淋巴細胞,其增殖能力明顯高于CXCL16(0 ng/ml),吸光度(A)值分彆為0.51±0.06、0.56±0.05、0.55±0.04、0.41±0.04(P＜0.05).併且CXCL16對CIA組小鼠淋巴細胞的增殖刺激能力明顯高于其對健康對照組小鼠淋巴細胞(P均＜0.05).③覈因子κB受體活化因子配體(RANKL)mRNA、IL-2和榦擾素-γ水平在CIA CXCL16(400、800 ng/ml)組均明顯高于CXCL16(0 ng/ml)組(P＜0.01).結論 CXCL16可能通過活化淋巴細胞在CIA髮病中髮揮重要作用.
목적 료해CXCL16재효원유도성관절염(CIA)소서발병중적작용.방법 이8지정상소서위대조,채용매련면역흡부시험(ELISA)화반전록-취합매련반응(RT-PCR)법,분별검측CXCL16재12지CIA소서외주혈중적단백수평급병변활막조직중적mRNA수평,재채용CCK-8법、RT-PCR화ELISA,분별검측불동농도적CXCL16중조단백(0,100,200,400,800 ng/ml)자격서비림파세포적증식정황、상청중백세포개소(IL)-2화간우소-γ수평급RANKL mRNA표체수평.채용t검험화단인소방차분석진행통계분석.결과 ①여대조조상비,CIA소서외주혈CXCL16[분별위(72±8)화(127±10)pg/ml,P＜0.05]화활막CXCL16 mRNA수평(분별위0.214±0.007화0.375±0.009,P＜0.01)균현저증고.②CXCL16(200、400、800 ng/ml)작용우CIA소서림파세포,기증식능력명현고우CXCL16(0 ng/ml),흡광도(A)치분별위0.51±0.06、0.56±0.05、0.55±0.04、0.41±0.04(P＜0.05).병차CXCL16대CIA조소서림파세포적증식자격능력명현고우기대건강대조조소서림파세포(P균＜0.05).③핵인자κB수체활화인자배체(RANKL)mRNA、IL-2화간우소-γ수평재CIA CXCL16(400、800 ng/ml)조균명현고우CXCL16(0 ng/ml)조(P＜0.01).결론 CXCL16가능통과활화림파세포재CIA발병중발휘중요작용.
Objective To investigate the effect of CXCL16 on the development of murine collageninduced arthritis (CIA). Methods CXCL16 mRNA of the involved synovium and serum CXCL16 protein were determined respectively by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay (ELISA) in murine collagen-induced arthritis. The proliferation of lymphocytes from murine spleen and the level of RANKL mRNA, stimulated by CXCL16 at different concentrations (0,100, 200, 400, 800 ng/ml), was detected respectively by CCK-8 and RT-PCR, then the level of IL-2 and IFN-γ in culture supernatant was detected by ELISA. Comparisons between groups were tested by t test and one-way ANOVA analysis. Results The serum CXCL16 [(127± 10) vs (72±8) pg/ml, P＜0.05] and synovial CXCL16 mRNA (0.214±0.007 vs 0.375±0.009, P＜0.01) in CIA were all significantly higher than those in normal controls. The proliferation of CXCL16 (200, 400, 800 ng/ml) in CIA mouse lymphocytes, was significantly higher than that of CXCL16 (0 ng/ml) (0.51±0.06, 0.56±0.05, 0.55±0.04, (0.41±0.04, P＜0.05). And CXCL16 on the CIA stimulated lymphocyte proliferation was significantly higher than controls on normal lymphocytes (P＜0.05). Compared with blank control group, the expression of IL-2, IFN-γ and RANKL mRNA of CIA CXCL16 (400, 800 ng/ml) groups was higher significantly (P＜0.01). Conclusion CXCL16 plays an important role in the development of murine CIA by activating lymphocytes.
