中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
11期
4849-4853
,共5页
朱蕾%李娟%武丹威%罗丽丰%郭磊%于晓丽%叶菜英%张德昌
硃蕾%李娟%武丹威%囉麗豐%郭磊%于曉麗%葉菜英%張德昌
주뢰%리연%무단위%라려봉%곽뢰%우효려%협채영%장덕창
NF-κB%肿瘤坏死因子α%细胞因子类%羧胺三唑%成纤维样滑膜细胞
NF-κB%腫瘤壞死因子α%細胞因子類%羧胺三唑%成纖維樣滑膜細胞
NF-κB%종류배사인자α%세포인자류%최알삼서%성섬유양활막세포
NF-kappa B%Tumor necrosis factor-alpha%Cytokines%Carboxyamidotriazole%Fibroblast-like synoviocyte
目的探讨羧胺三唑对TNF-α诱导的佐剂性关节炎大鼠成纤维样滑膜细胞分泌促炎细胞因子的影响及部分机制。方法用弗氏完全佐剂诱导大鼠佐剂性关节炎模型，分离培养的佐剂性关节炎成纤维样滑膜细胞用20 ng/ml TNF-α刺激并用不同浓度羧胺三唑（10、20、40μmol/L）处理。 ELISA法检测成纤维样滑膜细胞上清中IL-1β和IL-6含量， Western blot 法检测NF-κB p65的蛋白表达。结果经20 ng/ml TNF-α刺激后，成纤维样滑膜细胞分泌IL-1β和IL-6水平，以及细胞核中NF-κB p65的表达显著增加（ P＜0.01）。羧胺三唑（20、40μmol/L）能够显著抑制TNF-α诱导的IL-1β[（417.39±29.80）pg/ml vs．（264.63±9.35）pg/ml，（186.13±25.71）pg/ml，P＜0.01]和IL-6[（383.45±32.13）pg/ml vs．（248.39±30.51）pg/ml，（189.64±27.86）pg/ml，P＜0.01]分泌，且明显减少细胞核中NF-κB p65的表达（P＜0.01）。结论羧胺三唑可能通过抑制NF-κB活化来减少TNF-α诱导的佐剂性关节炎成纤维样滑膜细胞中促炎细胞因子IL-1β、IL-6的产生。
目的探討羧胺三唑對TNF-α誘導的佐劑性關節炎大鼠成纖維樣滑膜細胞分泌促炎細胞因子的影響及部分機製。方法用弗氏完全佐劑誘導大鼠佐劑性關節炎模型，分離培養的佐劑性關節炎成纖維樣滑膜細胞用20 ng/ml TNF-α刺激併用不同濃度羧胺三唑（10、20、40μmol/L）處理。 ELISA法檢測成纖維樣滑膜細胞上清中IL-1β和IL-6含量， Western blot 法檢測NF-κB p65的蛋白錶達。結果經20 ng/ml TNF-α刺激後，成纖維樣滑膜細胞分泌IL-1β和IL-6水平，以及細胞覈中NF-κB p65的錶達顯著增加（ P＜0.01）。羧胺三唑（20、40μmol/L）能夠顯著抑製TNF-α誘導的IL-1β[（417.39±29.80）pg/ml vs．（264.63±9.35）pg/ml，（186.13±25.71）pg/ml，P＜0.01]和IL-6[（383.45±32.13）pg/ml vs．（248.39±30.51）pg/ml，（189.64±27.86）pg/ml，P＜0.01]分泌，且明顯減少細胞覈中NF-κB p65的錶達（P＜0.01）。結論羧胺三唑可能通過抑製NF-κB活化來減少TNF-α誘導的佐劑性關節炎成纖維樣滑膜細胞中促炎細胞因子IL-1β、IL-6的產生。
목적탐토최알삼서대TNF-α유도적좌제성관절염대서성섬유양활막세포분비촉염세포인자적영향급부분궤제。방법용불씨완전좌제유도대서좌제성관절염모형，분리배양적좌제성관절염성섬유양활막세포용20 ng/ml TNF-α자격병용불동농도최알삼서（10、20、40μmol/L）처리。 ELISA법검측성섬유양활막세포상청중IL-1β화IL-6함량， Western blot 법검측NF-κB p65적단백표체。결과경20 ng/ml TNF-α자격후，성섬유양활막세포분비IL-1β화IL-6수평，이급세포핵중NF-κB p65적표체현저증가（ P＜0.01）。최알삼서（20、40μmol/L）능구현저억제TNF-α유도적IL-1β[（417.39±29.80）pg/ml vs．（264.63±9.35）pg/ml，（186.13±25.71）pg/ml，P＜0.01]화IL-6[（383.45±32.13）pg/ml vs．（248.39±30.51）pg/ml，（189.64±27.86）pg/ml，P＜0.01]분비，차명현감소세포핵중NF-κB p65적표체（P＜0.01）。결론최알삼서가능통과억제NF-κB활화래감소TNF-α유도적좌제성관절염성섬유양활막세포중촉염세포인자IL-1β、IL-6적산생。
Objective To investigate the effects of carboxyamidotriazole ( CAI ) on TNF-α-induced cytokines secretion in fibroblast-like synoviocytes ( FLS) from adjuvant arthritis ( AA) rats and its mechanisms. Methods Freund′s completed adjuvant was used to induce AA in rats .FLS from AA rats were stimulated with 20 ng/ml TNF-αand incubated with CAI at the concentrations of 10,20,40 μmol/L.The contents of IL-1βand IL-6 in the culture supernatant were determined by ELISA method ,and the expression of NF-κB p65 in the cell nucleus was measured by Western blot.Results TNF-αsignificantly increased the secretion of IL-1βand IL-6,and the nuclear expression of NF-κB p65 in the FLS(P<0.01).CAI(20,40 μmol/L)inhibited the productions of IL-1β[(417.39 ±29.80)pg/ml vs.(264.63 ±9.35)pg/ml,(186.13 ±25.71)pg/ml,P<0.01]and IL-6 [(383.45 ± 32.13)pg/ml vs.(248.39 ±30.51)pg/ml,(189.64 ±27.86)pg/ml,P<0.01]in TNF-α-induced FLS,and CAI (20,40 μmol/L) also inhibited NF-κB p65 expression in the nucleus of TNF-α-induced FLS ( P <0.01 ). Conclusion CAI attenuate the secretion of pro-inflammatory cytokines such as IL-1βand IL-6 through inhibiting the activation of NF-κB.
