Protective Effect of Nitric Oxide Against Lipopolysaccharide-induced Cytotoxicity in C6-glial Cell / 대한해부학회지

Nitric oxide (NO) is mainly involved in brain ischemic damage to elucidate the protective mechanism of NO pretreatment on ischemic-induced cytotoxicity. This study was investigated whether NO pretreatment inhibits the increase of iNOS expression by lipopolysaccharide (LPS) combined phorbol 12-myristate 13-acetate (PMA) via regulating NF-kB activation in C6 glial cells. C6 glial cells with LPS and PMA for 72 hours markedly induced NO, but sodium nitroprusside (SNP) (100 nM) pretreatment before exposure of LPS and PMA significantly supressed NO production, iNOS expression and NF-kB activation by LPS and PMA. In addition, LPS and PMA treatment for 72 hours induced severely cell death and LDH release from cell into media in C6 glial cells. However SNP pretreatment before treatment of LPS and PMA significantly protected LPS and PMA induced cytotoxicity. Treatment with LPS and PMA induced caspase 3 activation follewed by chromosomal condensation, and fragmentation of nuclei in C6 glial cells. SNP pretreatment before exposure to LPS and PMA supressed caspase 3 activation and inhibited chromosomal condensation and fragmentation of nuclei. From these above results, it is suggest that the protective effects of SNP pretreatment against LPS and PMA induced cytotoxicity may be mediated by inhibiting the expression of iNOS via regulating NF-kB activation.

The Effect of Protein Kinase C Pretreatment on Gliotoxin Induced Apoptosis in H9c2 Cells / 체질인류학회지

Aspergillus funigatus and other pathogenic fungi synthesize a toxic epidithi- odiopiperzine (ETP) metabolite called gliotoxin. Gliotoxin is an epidithiodiopiperzine compound which can both react with sulfhydryl groups and form hydrogen peroxide. The fungal toxin gliotoxin induces apoptotic cell death in a variety of cells. Apoptosis induced by gliotoxin need calcium but effect of calcium preconditioning is unknown by gliotoxin. We studied the effect of protein kinase C and calcium preconditioning on gliotoxin-induced apoptosis in H9c2 cell. PKC and calcium preconditiong inhibited DNA fragmentation by gliotoxin. From this above results suggest that gliotoxin induce apoptosis via caspase-3 activation, because caspase-3 inhibitor (DEVD-CHO) didn't induce apoptosis in gliotoxin treated H9c2 clls. Calcium and PKC preconditioning inhibit caspase-3 activation by gliotoxin. These data means that PKC preconditioning is related with caspase-3 regulate in gliotoxin-induced apoptosis.