1.Study on Enzymology and Morphology Effects of Extractions of Cyanobacteria on Primary Cultured Hepatocyte
Wei SHI ; Huigang ZHU ; Xiaorong YAN ; Al ET
Journal of Environment and Health 1992;0(05):-
Objective To make a further study on the character and mechanism of hepatotoxic effect of microcystin(MC),which stands for the extractions of cyanobacteria Methods The enzymology and morphology effects of different concentrations of 0.1,1,10 ?g/ml extractions of cyanobacteria on primary cultured hepatocyte were observed Results It was shown that the concentrations of LDH and AST increased in the culture medium after exposure to MC at concentrations of 0.1 ,1 and 10 ?g/ml No significant changes of concentrations of AKP, GGT, ALT and GSH were observed in the culture media of tested groups.An active proliferation of cultured hepatocytes with apopotosis or necrosis were observed in the center of the proliferation foci in the treated groups.Characterisitic morphological alterations such as irregular shape,cytoplasmic cavity,plasma membrane blebs and protrusions were viewed in scanning electronic microscope as well as in cultured cell. Conclusion The extractions of cyanobacteria could promote the proliferation of hepatocyte and might influence the physiological and biochemical function and the integrity of hepatocyte
2.Detection of Neuron-specific Enolase and Soluble Intercellar Adhesion Molecule-1 in Serum and Cerebrospinal Fluid in the Patients with Viral Encephalitis
Ning SHI ; Weijing QIN ; Hengchao GE ; Huigang ZHANG ; Shimei ZHANG ; Jiaping WANG
Journal of Medical Research 2006;0(12):-
Objective To investigate the changes of the neuron-specific enolase(NSE) and soluble intercellar adhesion molecule-1(CAM-1) in serum and cerebrospinal fluid(CSF) in the patients with viral encephhalites (VE). Methods The levels of NSE and sICAM-1 in serum and CSF were determined before and after treatment using ELISA in 58 patients with VE and 20 normal persons. Results The levels of NSE and sICAM-1 in serum before treatment were obviously higher than those of control group, and their differences were significant (P0.05). Conclusions NSE and sICAM-1 may contribute to pathologic course in infection of VE and the levels of NSE and sICAM-1 in serum and CSF may serve as markers of differential diagnosis and clinical significance.
3.Hsa-miR-218 inhibits growth of cervical cancer HeLa cells by targeting to LASP1
Yu QIU ; Jianping HUANG ; Qinxian ZHOU ; Huan WANG ; Huigang SHI ; Jinhua HE
Chinese Journal of Pathophysiology 2015;(9):1572-1577
AIM:To study the effect of hsa-miR-218 on cervical cancer HeLa cell growth and the underlying molecular mechanism .METHODS:The lentivirus expression vector pmiR-218 targeting to hsa-miR-218 was constructed . pmiR-218 was transfected into HeLa cells .The number of viable HeLa cells was counted by the method of Trypan blue ex-clusion.The inhibitory rate of cell activity was detected by WST-8 assay.The expression of LIM and SH3 protein 1 (LASP1) at mRNA and protein levels was determined by real-time PCR and Western blot.The interaction between miR-218 and LASP1 was examined using a luciferase reporter assay .RESULTS:The lentivirus expression vector pmiR-218 tar-geting to hsa-miR-218 was constructed successfully and confirmed by DNA sequencing .Over-expression of miR-218 inhibi-ted the activity of HeLa cells with the inhibitory rates of 15%, 26%and 65%at 24 h, 48 h and 72 h, respectively .The difference between transfection group and blank control /negative control group was statistically significant .The luciferase activity was reduced when co-transfection with miR-218 mimics and LASP1-3’ UTR plasmid.The relative expression of miR-218 was increased after transfection with pmiR-218.Over-expression of miR-218 down-regulated the LASP1 expression at mRNA and protein levels by 25%and 75%respectively.Compared with blank control group and negative control group , the difference was statistically significant (P<0.05).CONCLUSION:pmiR-218 effectively inhibits the growth of HeLa cells in a time-dependent manner.miR-218 targets to the 3’UTR of LASP1, thus down-regulating the expression of LASP1 in HeLa cells .