中国临床药理学杂志
中國臨床藥理學雜誌
중국림상약이학잡지
THE CHINESE JOURNAL OF CLINICAL PHARMACOLOGY
2014年
7期
597-600
,共4页
沙利度胺%肝细胞癌%化疗%增敏作用%血管内皮细胞生长因子
沙利度胺%肝細胞癌%化療%增敏作用%血管內皮細胞生長因子
사리도알%간세포암%화료%증민작용%혈관내피세포생장인자
thalidomide%hepatocellular carcinoma%chemotherapy%sen-sitization effect%vascular endothelial growth factor
目的：观察沙利度胺对肝癌细胞HepG2化疗效果的影响。方法吉西他滨（0.30，1.25μg· mL-1）与沙利度胺（15.62μg· mL-1）联合处理HepG2肝癌细胞24 h，用MTT法测定细胞的增殖情况；Hoechst 33342染色检测细胞形态改变；用RT-PCR与免疫细胞化学法检测血管内皮细胞生长因子（ VEGF ） mRNA及蛋白表达。结果吉西他滨能浓度依赖性抑制HepG2细胞的增殖，而沙利度胺对其存活率影响不明显；与单用吉西他滨相比，两药联用对细胞增殖的抑制作用明显增加（ P﹤0.05），且HepG2对吉西他滨敏感性的作用显著增加；两药联用可诱导HepG2细胞凋亡，导致HepG2细胞核形态改变更明显；与单用吉西他滨相比，两药联用后能明显下调VEGF在细胞的表达水平，且两药合用对VEGF表达的影响也有协同作用。结论沙利度胺可能通过下调VEGF表达以增加肝癌细胞HepG2对吉西他滨化疗的敏感性。
目的：觀察沙利度胺對肝癌細胞HepG2化療效果的影響。方法吉西他濱（0.30，1.25μg· mL-1）與沙利度胺（15.62μg· mL-1）聯閤處理HepG2肝癌細胞24 h，用MTT法測定細胞的增殖情況；Hoechst 33342染色檢測細胞形態改變；用RT-PCR與免疫細胞化學法檢測血管內皮細胞生長因子（ VEGF ） mRNA及蛋白錶達。結果吉西他濱能濃度依賴性抑製HepG2細胞的增殖，而沙利度胺對其存活率影響不明顯；與單用吉西他濱相比，兩藥聯用對細胞增殖的抑製作用明顯增加（ P﹤0.05），且HepG2對吉西他濱敏感性的作用顯著增加；兩藥聯用可誘導HepG2細胞凋亡，導緻HepG2細胞覈形態改變更明顯；與單用吉西他濱相比，兩藥聯用後能明顯下調VEGF在細胞的錶達水平，且兩藥閤用對VEGF錶達的影響也有協同作用。結論沙利度胺可能通過下調VEGF錶達以增加肝癌細胞HepG2對吉西他濱化療的敏感性。
목적：관찰사리도알대간암세포HepG2화료효과적영향。방법길서타빈（0.30，1.25μg· mL-1）여사리도알（15.62μg· mL-1）연합처리HepG2간암세포24 h，용MTT법측정세포적증식정황；Hoechst 33342염색검측세포형태개변；용RT-PCR여면역세포화학법검측혈관내피세포생장인자（ VEGF ） mRNA급단백표체。결과길서타빈능농도의뢰성억제HepG2세포적증식，이사리도알대기존활솔영향불명현；여단용길서타빈상비，량약련용대세포증식적억제작용명현증가（ P﹤0.05），차HepG2대길서타빈민감성적작용현저증가；량약련용가유도HepG2세포조망，도치HepG2세포핵형태개변경명현；여단용길서타빈상비，량약련용후능명현하조VEGF재세포적표체수평，차량약합용대VEGF표체적영향야유협동작용。결론사리도알가능통과하조VEGF표체이증가간암세포HepG2대길서타빈화료적민감성。
Objective To investigate the chemotherapy sensitization effect of thalidomide on hepatocellular carcinoma cell HepG 2.Methods With gemcitabine ( 0.30, 1.25 μg · L-1 ) and thalidomide ( 15.62μg· mL-1 ) treating HepG2 for 24 h, the cell viability of HepG2 was measured with MTT assay.Morphological change of cell nucleus was de-tected with Hoechst 33342 staining.By RT-PCR and immunocytochemistry method to detect vascular endothelial growth factor (VEGF) mRNA and pro-tein expression.Results Gemcitabine could suppress the proliferation of HepG2 with concentration dependence , but little effect of thalidomide on the survival of the degrees of HepG 2.Compared with gemcitabine alone , combi-nation of the two drugs on inhibition of cell proliferation significantly in-creased (P<0.05), and the HepG2 sensitivity to gemcitabine is increased significantly.Sally degrees of combination of the two drugs on HepG 2 cells induced apoptosis , lead to HepG2 nuclear shape changed.Compared with gemcitabine alone , degree of combination of the two drugs on inhibition could be significantly lowered after the expression of VEGF in cells , and appeared to have synergy effects on the protein expression.Conclusion Thalidomide can increase HepG2 sensitivity to chemotherapy of gemcitabine and its mechanism may be associated with lower VEGF expression.
