• Biomedical Science Letters
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• v.12 no.2
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• pp.81-89
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• 2006

The ischemia-responsive 94 gene (irp94) encoding a 94 kDa endoplasmic reticulum resident protein was investigated its molecular properties associated with unfoled protein responses. First, the expression of irp94 mRNA was tested after the reperfusion of the transient forebrain ischemia induction at the central nervous system in three Mongolian gerbils. Second, irp94 expression in PC12 cells, which are derived from transplantable rat pheochromocytoma cultured in the DMEM media, was tested at transcriptional and translational levels. The half life of irp94 mRNA was also determined In PC12 cells. Last, the changes of irp94 mRNA expression were investigated by the addition of various ER stress inducible chemicals (A23187, BFA, tunicamycin, DTT and $H_2O_2$) and proteasome inhibitors, and heat shock. High level expression of irp94 mRNA was detected after 3 hours reperfusion in the both sites of the cerebral cortex and hippocampus of the gerbil brain. The main regulation of irp94 mRNA expression in PC 12 cells was determined at the transcriptional level. The half life of irp94 mRNA in PC12 cells was approximately 5 hours after the initial translation. The remarkable expression of irp94 mRNA was detected by the treatment of tunicamycin, which blocks glycosylation of newly synthesized polypeptides, and $H_2O_2$, which induces apoptosis. When PC12 cells were treated with the cytosol proteasome inhibitors such as ALLN (N-acetyl-leucyl-norleucinal) and MG 132 (methylguanidine), irp94 mRNA expression was increased. These results indicate that expression of irp94 was induced by ER stress including oxidation condition and glycosylation blocking in proteins. Expression of irp94 was increased when the cells were chased after heat shock, suggesting that irp94 may be involved in recovery rather than protection against ER stresses. In addition, irp94 expression was remarkably increased when cytosol proteasomes were inhibited by ALLN and MG 132, suggesting that irp94 plays an important role for maintaining the ERAD (endoplasmic reticulum associated degradation) function.

• Journal of Oriental Physiology
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• v.14 no.2 s.20
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• pp.199-208
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• 1999

As the average life span have been lengthened and the rate of senile population have been raised, chronic degenerative diseases incident to aging has been increased rapidly and become a social problem. With this social background, recently, the facts that oxygen radicals(OR) have toxic effects on Central Nervous System and Peripheral Nervous System and cause neuropathy such as Parkinson's Disease, Alzheimer Disease have been turned out, and accordingly lots of studies on the mechanism of the toxic effects of OR on nerves, the diseases caused by OR and the approaches to curing the diseases have been made. The purpose of this study is to examine the toxic effects caused by Glucose Oxidase(GO) and the effects of herbal extracts such as Chilbokyeum(CBY) on the treatment of the toxic effects. For this purpose, experiments with the cultured cell from the cerebrums of new born mice were done. The results of these experiments were as follows. 1. GO, a oxygen radical, decreased the survival rate of the cultured cells on NR assay and MTT assay 2. GO, a oxygen radical, increased lipid peroxidation and the amount of LDH. 3. CBY have efficacy of decreasing lipid peroxidation. 4. CBY have efficacy of decreasing the amount of LOH. From the above results, It is concluded that Chilbokyeum has marked efficacy as a treatment for the damages caused in the GO-mediated oxidative process. And Chilbokyeum is thought to have certain pharmacological effects on controlling over aging and treating Dementia. Further clinical study of this pharmacological effects of Chilbokyeum should be complemented.

• Journal of Oriental Physiology
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• v.14 no.2 s.20
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• pp.117-126
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• 1999

The purpose of this study is to examine the toxic effects caused by Glucose Oxidase(GO) and the effects of herbal extracts such as Acori Rhizoma(AR) on the treatment of the toxic effects. For this purpose, experiments with the cultured cell from the cerebrums of new born mice were done. The results of these experiments were as follows. 1. GO, a oxygen radical, decreased the survival rate of the cultured cells on NR assay and MTT assay. 2. GO, a oxygen radical, decreased the amount of neurofilaments and total protein. 3. AR have efficacy of increasing the amount of neurofilament. 4. AR have efficacy of increasing the amount of total protein. From the above results, It is concluded that AR has marked efficacy as a treatment for the damages caused in the GO-mediated oxidative process. And AR is thought to have certain pharmacological effects on controlling over aging. Further clinical study of this pharmacological effects of AR should be complemented.