世界科学技术-中医药现代化
世界科學技術-中醫藥現代化
세계과학기술-중의약현대화
WORLD SCIENCE AND TECHNOLOGY-MODERNIZATION OF TRADITIONAL CHINESE MEDICINE
2014年
3期
582-586
,共5页
昆山合剂%类风湿关节炎%贫血%滑膜成纤维细胞%MyD88%IL-6
昆山閤劑%類風濕關節炎%貧血%滑膜成纖維細胞%MyD88%IL-6
곤산합제%류풍습관절염%빈혈%활막성섬유세포%MyD88%IL-6
Kunshan Mixture%rheumatoid arthritis%anemia%fibroblast-like synoviocytes%MyD88%IL-6
探讨昆山合剂（昆明山海棠、山血丹组成）对体外培养的类风湿关节炎（RA）致慢性病贫血患者滑膜成纤维细胞（FLS）增殖以及人类髓样分化蛋白88（MyD88）mRNA及其下游因子IL-6表达的影响和机制。方法：制备甲氨蝶呤和昆山合剂高、中、低剂量组的家兔含药血清；离体培养RA-FLS，取第3至5代细胞加入各组含药血清干预，MTT法检测各含药血清组和对照组RA-FLS的增殖情况，RT-PCR检测含药血清对该细胞MyD88 mRNA表达的影响。结果：干预24、48、72 h之后，与空白组比较，各浓度组的昆山合剂组和甲氨蝶呤含药血清作用均能明显抑制RA-FLS增殖（P<0.05），对脂多糖诱导的MyD88 mRNA高表达也有明显抑制作用（P<0.05），与脂多糖诱导组比较，48 h后昆山合剂高剂量组细胞培养上清的IL-6含量明显降低（P<0.05）。结论：昆山合剂含药血清能显著抑制RA-FLS增殖，并可下调脂多糖诱导的TLR4 mRNA及其下游炎症因子IL-6的表达，这可能为该方治疗RA的机制之一。
探討昆山閤劑（昆明山海棠、山血丹組成）對體外培養的類風濕關節炎（RA）緻慢性病貧血患者滑膜成纖維細胞（FLS）增殖以及人類髓樣分化蛋白88（MyD88）mRNA及其下遊因子IL-6錶達的影響和機製。方法：製備甲氨蝶呤和昆山閤劑高、中、低劑量組的傢兔含藥血清；離體培養RA-FLS，取第3至5代細胞加入各組含藥血清榦預，MTT法檢測各含藥血清組和對照組RA-FLS的增殖情況，RT-PCR檢測含藥血清對該細胞MyD88 mRNA錶達的影響。結果：榦預24、48、72 h之後，與空白組比較，各濃度組的昆山閤劑組和甲氨蝶呤含藥血清作用均能明顯抑製RA-FLS增殖（P<0.05），對脂多糖誘導的MyD88 mRNA高錶達也有明顯抑製作用（P<0.05），與脂多糖誘導組比較，48 h後昆山閤劑高劑量組細胞培養上清的IL-6含量明顯降低（P<0.05）。結論：昆山閤劑含藥血清能顯著抑製RA-FLS增殖，併可下調脂多糖誘導的TLR4 mRNA及其下遊炎癥因子IL-6的錶達，這可能為該方治療RA的機製之一。
탐토곤산합제（곤명산해당、산혈단조성）대체외배양적류풍습관절염（RA）치만성병빈혈환자활막성섬유세포（FLS）증식이급인류수양분화단백88（MyD88）mRNA급기하유인자IL-6표체적영향화궤제。방법：제비갑안접령화곤산합제고、중、저제량조적가토함약혈청；리체배양RA-FLS，취제3지5대세포가입각조함약혈청간예，MTT법검측각함약혈청조화대조조RA-FLS적증식정황，RT-PCR검측함약혈청대해세포MyD88 mRNA표체적영향。결과：간예24、48、72 h지후，여공백조비교，각농도조적곤산합제조화갑안접령함약혈청작용균능명현억제RA-FLS증식（P<0.05），대지다당유도적MyD88 mRNA고표체야유명현억제작용（P<0.05），여지다당유도조비교，48 h후곤산합제고제량조세포배양상청적IL-6함량명현강저（P<0.05）。결론：곤산합제함약혈청능현저억제RA-FLS증식，병가하조지다당유도적TLR4 mRNA급기하유염증인자IL-6적표체，저가능위해방치료RA적궤제지일。
This study was aimed to investigate the effects and mechanisms of serum containing Kunshan Mixture (KSM) on in vitro proliferation of fibroblast-like synoviocytes(FLS) and myeloid differentiation protein 88 (MyD88) mRNA and the expression of its downstream factor IL-6 in rheumatoid arthritis patients with chronic anemia. Rabbit medicated serum containing methotrexate (MTX) and KSM of high-, medium-, and low-dose were pre-pared. In vitro culture of RA-FLS was given. Cells from the 3rd to 5th generation were intervened with medicat-ed serum of different groups. MTT method was used in the detection of RA-FLS proliferation condition among different medicated serum groups and the control group . RT-PCR was used in the detection of MyD88 mRNA ex-pression of these cells. The results showed that compared with the blank control group, after the intervention of 24 , 48 , or 72 h , KSM of different concentrations and MTX medicated serum had obvious inhibitive effects on the proliferation of RA-FLS (P < 0.05). It also had obvious inhibitive effects on the high level expression of LPS-induced MyD88 mRNA (P < 0.05). Compared with the LPS-induced group, the supernatant IL-6 content was ob-viously reduced in the KSM of high-dose group after 48 h ( P < 0 . 05 ) . It was concluded that KSM medicated serum can obviously inhibit the proliferation of RA-FLS and downregulate the expression of LPS-induced TLR4mRNA and its downstream inflammatory factor IL-6. It may be one of the mechanisms for RA treatment with this prescription .
