中国中医药信息杂志
中國中醫藥信息雜誌
중국중의약신식잡지
CHINESE JOURNAL OF INFORMATION ON TRADITIONAL CHINESE MEDICINE
2013年
11期
25-27
,共3页
姜黄素%肿瘤坏死因子-α%核转录因子-κB%核转录因子抑制蛋白-Bα%Hepg-2细胞
薑黃素%腫瘤壞死因子-α%覈轉錄因子-κB%覈轉錄因子抑製蛋白-Bα%Hepg-2細胞
강황소%종류배사인자-α%핵전록인자-κB%핵전록인자억제단백-Bα%Hepg-2세포
curcumin%TNF-α%NF-κB%Iκ-Bα%Hepg-2
目的观察姜黄素对经肿瘤坏死因子-α(TNF-α)诱导后人肝癌细胞(Hepg-2)核转录因子(NF-κB)及其抑制蛋白-Bα(Iκ-Bα)表达的影响,探讨其对非酒精性脂肪性肝炎的影响。方法将Hepg-2细胞用含10%胎牛血清的DMEM培养基培养,细胞分为6组,即正常对照组、TNF-α组、2.5μmol/L姜黄素组、5μmol/L姜黄素组、10μmol/L姜黄素组、20μmol/L姜黄素组。MTT检测姜黄素对Hepg-2细胞增殖活力,Western blotting法检测NF-κB及IκB-Bα蛋白的变化。结果 Hepg-2细胞经 TNF-α刺激后,NF-κB 表达增强,与正常对照组比较差异有统计学意义(P<0.05),而IκB-α表达虽增加但与正常对照组比较差异无统计学意义;经姜黄素干预后,NF-κB表达明显减弱,而IκB-Bα表达明显增强,与TNF-α组比较差异有统计学意义(P<0.05)。结论姜黄素可拮抗TNF-α诱导的NF-κB炎性信号通路的激活,从而减轻肝细胞的炎性损伤。
目的觀察薑黃素對經腫瘤壞死因子-α(TNF-α)誘導後人肝癌細胞(Hepg-2)覈轉錄因子(NF-κB)及其抑製蛋白-Bα(Iκ-Bα)錶達的影響,探討其對非酒精性脂肪性肝炎的影響。方法將Hepg-2細胞用含10%胎牛血清的DMEM培養基培養,細胞分為6組,即正常對照組、TNF-α組、2.5μmol/L薑黃素組、5μmol/L薑黃素組、10μmol/L薑黃素組、20μmol/L薑黃素組。MTT檢測薑黃素對Hepg-2細胞增殖活力,Western blotting法檢測NF-κB及IκB-Bα蛋白的變化。結果 Hepg-2細胞經 TNF-α刺激後,NF-κB 錶達增彊,與正常對照組比較差異有統計學意義(P<0.05),而IκB-α錶達雖增加但與正常對照組比較差異無統計學意義;經薑黃素榦預後,NF-κB錶達明顯減弱,而IκB-Bα錶達明顯增彊,與TNF-α組比較差異有統計學意義(P<0.05)。結論薑黃素可拮抗TNF-α誘導的NF-κB炎性信號通路的激活,從而減輕肝細胞的炎性損傷。
목적관찰강황소대경종류배사인자-α(TNF-α)유도후인간암세포(Hepg-2)핵전록인자(NF-κB)급기억제단백-Bα(Iκ-Bα)표체적영향,탐토기대비주정성지방성간염적영향。방법장Hepg-2세포용함10%태우혈청적DMEM배양기배양,세포분위6조,즉정상대조조、TNF-α조、2.5μmol/L강황소조、5μmol/L강황소조、10μmol/L강황소조、20μmol/L강황소조。MTT검측강황소대Hepg-2세포증식활력,Western blotting법검측NF-κB급IκB-Bα단백적변화。결과 Hepg-2세포경 TNF-α자격후,NF-κB 표체증강,여정상대조조비교차이유통계학의의(P<0.05),이IκB-α표체수증가단여정상대조조비교차이무통계학의의;경강황소간예후,NF-κB표체명현감약,이IκB-Bα표체명현증강,여TNF-α조비교차이유통계학의의(P<0.05)。결론강황소가길항TNF-α유도적NF-κB염성신호통로적격활,종이감경간세포적염성손상。
Objective To investigate the effect of curcumin on the expression of nuclear transcription factor (NF-kappa B) and its inhibitory protein (Iκ-Bα) in liver cancer cells (Hepg-2) induced by TNF-α, and explore its effect on non-alcoholic steatohepatitis. Methods The cells were divided into normal group, TNF-alpha group, and different concentrations of curcumin treatment group. MTT and Western blotting were used to assay curcumin’s effect on Hepg-2 proliferation activity and changes of NF-κB and Iκ-Bα’s in Hepg-2. Results Compared with the normal group, TNF-αgroup enhanced NF-κB and Iκ-Bαexpression, but the increase of Iκ-Bα had no statistical significance (P>0.05). Curcumin treatment group’s NF-κB expression was significantly weakened than TNF-α group, while Iκ-Bα was significantly enhanced than that of TNF-α group. Conclusion Curcumin can antagonize NF-κB inflammatory signaling pathway activation induced by TNF-α, thus reduce the inflammatory injury of the liver cells.