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1.
Chinese Journal of Pathophysiology ; (12): 1619-1624, 2017.
Artigo em Chinês | WPRIM | ID: wpr-660819

RESUMO

AIM:To investigate the effects of indoleamine 2,3-dioxygenase 2 (IDO2) silencing on proliferation,migration and invasion of B16-BL6 melanoma cells.METHODS:IDO2-siRNA was transfected into the B16-BL6 melanoma cells in vitro.The expression of IDO2 or IDOl at mRNA and protein levels was detected by real-time PCR and Western blot.Colony formation assay was performed to analyze the proliferation of IDO2-silencing tumor cells.The migration ability of B16-BL6 cells after silencing of IDO2 was measured by wound healing assay and Transwell cell migration assay.The invasion ability of the tumor cells was detected by Transwell cell invasion assay.RESULTS:IDO2-siRNA significantly down-regulated IDO2 expression in B16-BL6 melanoma cells,and did not affect IDO1 expression.Compared with control group,the colony formation ability,the migratory distance measured by wound healing assay,and the migration and the invasion cell numbers detected by Transwell assay all remarkably decreased in the IDO2-silencing cells.CONCLUSION:IDO2 silencing affects the proliferation,migration and invasion abilities of the R16-BL6 melanoma cells.

2.
Chinese Journal of Pathophysiology ; (12): 1619-1624, 2017.
Artigo em Chinês | WPRIM | ID: wpr-662825

RESUMO

AIM:To investigate the effects of indoleamine 2,3-dioxygenase 2 (IDO2) silencing on proliferation,migration and invasion of B16-BL6 melanoma cells.METHODS:IDO2-siRNA was transfected into the B16-BL6 melanoma cells in vitro.The expression of IDO2 or IDOl at mRNA and protein levels was detected by real-time PCR and Western blot.Colony formation assay was performed to analyze the proliferation of IDO2-silencing tumor cells.The migration ability of B16-BL6 cells after silencing of IDO2 was measured by wound healing assay and Transwell cell migration assay.The invasion ability of the tumor cells was detected by Transwell cell invasion assay.RESULTS:IDO2-siRNA significantly down-regulated IDO2 expression in B16-BL6 melanoma cells,and did not affect IDO1 expression.Compared with control group,the colony formation ability,the migratory distance measured by wound healing assay,and the migration and the invasion cell numbers detected by Transwell assay all remarkably decreased in the IDO2-silencing cells.CONCLUSION:IDO2 silencing affects the proliferation,migration and invasion abilities of the R16-BL6 melanoma cells.

3.
Chin. j. integr. med ; Chin. j. integr. med;(12): 201-206, 2016.
Artigo em Inglês | WPRIM | ID: wpr-229543

RESUMO

<p><b>OBJECTIVE</b>To explore the neuroprotective effects of baicalin against hypoxia and glucose deprivation-reperfusion (OGD/RO)-induced injury in SH-SY5Y cells.</p><p><b>METHODS</b>SH-SY5Y cells were divided into a control group, a OGD/RO group, which was subject to OGD/RO induction; and 3 baicalin groups subject to baicalin (1, 5, 25 μmol/L) for 2 h before induction of OGD/RO (low-, medium-, and high-dose baicalin groups). Cell viability was detected by thiazolyl blue tetrazolium bromide (MTT) assay and flow cytometric analysis was used to detect cell apoptosis. Real-time polymerase chain reaction was performed to determine the mRNA expression of caspase-3 gene. Western blot analysis was conducted to determine the expression of nuclear factor (NF)-κB and N-methyl-daspartic acid receptor-1 (NMDAR1).</p><p><b>RESULTS</b>Baicalin could significantly attenuate OGD/RO mediated apoptotic cell death in SH-SY5Y cells; the apoptosis rates in the low-, medium- and high-dose groups were 12.1%, 7.9%, and 5.4%, respectively. Western blot and real-time PCR analysis revealed that significant decrease in caspase-3 expression in the baicalin group compared with the OGD/RO group (P<0.01). Additionally, down-regulation of NF-κB and NMDAR1 was observed in the baicalin group compared with those obtained from the OGD/RO group. Compared with the low-dose baicalin group, remarkable decrease was noted in the medium- and high-dose groups (P<0.01).</p><p><b>CONCLUSION</b>Baicalin pre-treatment attenuates brain ischemia reperfusion injury by suppressing cellular apoptosis.</p>


Assuntos
Humanos , Apoptose , Caspase 3 , Genética , Metabolismo , Morte Celular , Hipóxia Celular , Linhagem Celular Tumoral , Sobrevivência Celular , Flavonoides , Farmacologia , Glucose , Metabolismo , NF-kappa B , Metabolismo , Proteínas do Tecido Nervoso , Metabolismo , RNA Mensageiro , Genética , Metabolismo , Reação em Cadeia da Polimerase em Tempo Real , Receptores de N-Metil-D-Aspartato , Metabolismo , Reperfusão
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