Objective To investigate the relationship of hypoxia inducible factor-1 α(HIF-1α),tumor necrosis factor-α (TNF-α),hepatocyte growth factor (HGF) and cerebral infarction.Method Two hundred and twelve cases with acute cerebral infarction in the Fourth People's Hospital of Langfang from Jun.to Dec.2013 were divided into progressive cerebral infarction(PCI) group(n =105) and the stability of cerebral infarction (SCI) group (n =107).Meanwhile 100 healthy people were served as control group.Enzyme-linked immunosorbent assay(ELISA) was applied to detect the levels of HIF-1 α,TNF-α and HGF.The PCI group were divided into small groups according to nerve function or infarction lesion size,and the levels of HIF-1 α,TNF-α and HGF of each group.Result The levels of HIF-1 α,TNF-α,HGF in PCI group were (2.3 ± 1.3) ng/L,(4.0 ± 0.5) mg/L and (1.4 ± 0.3) μg/L,significantly higher than those in SCI group ((1.1 ± 0.5) ng/L,(3.1 ±1.3) mg/L and (0.7 ±0.4) μg/L;F=5.42) and control group((0.5 ±0.1) ng/L,(1.8 ±0.4) mg/L and (0.4 ±0.1) μg/L;F =3.14).Meanwhile,the levels of HIF-1 α,TNF-α,HGF in SCI group was significantly higher than that of the control group (F =1.32,P ＜ 0.05).The levels of HIF-1α,TNF-α,HGF in mild PCI group were significantly lower than those in moderate group and severe group,and those in moderate group was lower than those in severe group (F =0.93,4.32,2.31 ; P ＜ 0.01).The levels of HIF-1 α,TNF-α,HGF in small infarction group were (0.6 ± 0.4) ng/L,(2.7 ± 0.4) mg/L,(0.7 ± 0.4) μg/L,significantly lower than those in infarction group ((1.1 ± 0.5) ng/L,(4.4 ± 0.5) mg/L,(1.1 ± 0.2) μg/L; F =4.71,P＜0.05) and large infarction group((1.4 ± 0.6) ng/L,(4.8 ± 0.6) mg/L,(1.9 ± 0.5) μg/L; F =2.09,P＜0.05).The levels of HIF-1α,TNF-α,HGF in focal infarction group was significantly lower than that in large infarction group and the difference is statistically significant(F =2.45,P ＜0.05).Conclusion HIF-1 α,TNF-α and HGF serum levels in progressive cerebral infarction are significantly increased,which is related to the function defect and size of infarction.

Objective The purpose of this study is to investigate the apoptosis mechanisms of glioblasto-ma cell line U87 induced by sodium cantharidinate ( SCA) in vitro.Methods Growth inhibition of U87 by 0.625μg/mL,1.25μg/mL,2.5μg/mL,5μg/mL SCA at 24 h,48 h,72 h were analyzed by MTT assay respec-tively.Morphological changes of U 87 nuclear were detected by fluorescence microscope .U87 cell apoptosis and cell cycle arrest were detected after SCA treatment for 24 h and 48 h by flow cytometry.The changes of apoptosis-related genes Bcl -2,Bax,Caspase-3 expression were analyzed after 24 h of SCA treatment by RT -PCR as-say.Results MTT assay showed that growth inhibition of U 87 cell induced by SCA was accompanied with the in-creased drug concentration ,Hoechst33258 staining showed the morphology of apoptotic U 87 cells nucleui ,chromo-some condensation ,nuclear condensation ,some nuclear fragmentation and formation of apoptotic bodies .Flow cy-tometry showed that SCA could induce cell cycle arrest at the G 2/M phase,and could induce apoptosis of U87.RT-PCR results showed that after 24 h of SCA treatment caspase -3,bax expression of U87 was significantly higher than the control group(P<0.05),bcl-2 expression was significantly decreased (P<0.05),and P53 expression was not significantly increased(P>0.05).Conclusion Our results demonstrate that SCA can inhibit U87 pro-liferation and induce apoptosis of U 87 .