• The Korea Journal of Herbology
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• v.27 no.2
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• pp.77-83
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• 2012

Objectives : This work was designed to investigate the effect of The root of Achyranthes japonica Nakai (AJN) water extract on serum deprivation reperfusion-induced apoptosis in PC-12 cells and transient middle cerebral artery occlusion (tMCAO)-induced ischemic brains of rats. Methods : Apoptosis in PC12 cells was induced by serum deprivation and reperfusion. The cells were treated with AJN water extract at doses of 0.5 and 1.0 mg/ml for 24 hr after inducing the apoptosis. Cell viability was determined by WST-1 assay. The expression of caspase-3 protein was determined by Western blot. Ischemic brains were prepared from tMCAO-induced ischemic rats after oral administration with AJN at dose of 50 and 100 mg/kg, and then brain infarction was measured by TTC staining. Results : AJN significantly increased the cell viability in apoptocic-induced PC-12 cells, and also decreased the expression of caspase-3 protein. Furthermore, the administration of AJN significantly inhibited tMCAO-induced brain infarction in rats. Conclusions : Our results suggest that AJN extract has a neuroprotective property via suppressing the apoptosis in PC12 cells and the infarction of ischemic brains.

• Herbal Formula Science
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• v.13 no.1
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• pp.35-48
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• 2005

Alzheimer's disease(AD) is a geriatric dementia that is widespread in old age. In the near future AD will be the biggest problem in public health service. It has been widely believed that $A{\beta}$ peptide devided from APP causes apoptotic neurotoxicity in brain. However, recent evidence suggests that n99 may be an important factor causing neurotoxicity in AD. Mouse PC12 cells expressed with n99 exhibited remarkable apoptotic cell damage. We invesgated the protective effects of Gagamgobonhwan water extract(GKG). Findings from our experiments have shown that GKG inhibits the activities of CT99, which has neurotoxicities and apoptotic activities in cell line. In addition, treatment of GKG($75{\mu}g/ml$ 24 hours) partially prevented CT99-induced cytotoxicity in PC12 cells. As the result of this study, in GKG group the apoptosis in the nervous system was inhibited, the repair against the degerneration of PC12 cells by CT99 expression is promoted. Taken together, GKG exhibited inhibition of CT99-induced apoptotic cell death. GKG may be beneficial for the treatment of AD.

• Journal of the Korean Applied Science and Technology
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• v.36 no.2
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• pp.468-478
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• 2019

The aim of this study is to evaluate the efficacy of cordyceps militaris extracts for the improvement of cognitive dysfunction in PC12 and BV2 cells. Cordyceps militaris extracts was prepared by extracting with distilled water. Cell viability was assessed by MTT assay using PC12 cells and BV2 cells. Confirmed effects of L-glutamate induced cytotoxicity test, Acetylcoline (ACh) concentration, and Acetylcolinestase (AChE) activity in PC12 cells. Anti-inflammatory activities of cordyceps militaris extracts was measured through changes in the levels of nitric oxide (NO), and prostaglandin E2 ($PGE_2$) on lipopolysaccharide(LPS)-induced BV2 cell. In addition, we measured the expression of $NF-{\kappa}B$, p38, JNK, and caspase-3 in western blot analysis. Cordyceps militaris extracts showed no cytotoxicity at the concentrations of 1, 10, and $100{\mu}g/m{\ell}$ except for the concentration of $200{\mu}g/m{\ell}$. Cordyceps militaris extracts protected the cell and exhibited significant increases in the ACh concentration and a significant decrease in the AChE activity in L-glutamate induced PC12 cells. Moreover, cordyceps militaris extracts inhibited the productions NO, and PGE2 level and the protein expression of $NF-{\kappa}B$, p38, JNK, caspase-3 in LPS-induced BV2 cells. These results indicate that cordyceps militaris extracts possible prevented and improved cognitive dysfuction symptoms. Thus, cordyceps militaris extracts may be a novel natural material option for the improvement of cognitive dysfunction.

• BMB Reports
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• v.41 no.12
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• pp.840-845
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• 2008

Nucleophosmin/B23, a major nucleolar phosphoprotein, is overexpressed in actively proliferating cells. In this study, we demonstrate that B23 exclusively localizes in the nucleolus, whereas ATP depletion results in the redistribution of B23 throughout the whole nucleus and destabilizes B23 via caspase-3 mediated cleavage. Interestingly, ATP binding precedes PI(3,4,5)P3 binding at lysine 263 and ATP binding mutants fail to restore the anti-apoptotic functions of B23 in PC12 cells. Thus, the ATP-B23 interaction is required for the stability of the B23 protein and regulates cell survival, confining B23 within the nucleolus in PC12 cells.

• Journal of Oriental Neuropsychiatry
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• v.18 no.1
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• pp.63-78
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• 2007

Objective : This experiment was designed to investigate the effect of Thalictrum foetidum(TFD) on the Alzheimer's disease. Method : The effects of TFD on amyloid precursor proteins(APP), acetylcholinesterase(AChE), glial fibrillary acidic protein(GFAP) mRNA of PC-12 cell treated by amyloid ${\beta}$ $protein(A{\beta})$ and $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ mRNA of THP-l cell treated by lipopolysaccharide(LPS), AChE activity of PC-12 cell lysate treated by $A{\beta}$ and behavior of the memory deficit mice induced by scopolamine, and glucose, AChE in serum of the memory deficit mice induced by scopolamine were investigated, respectively. Results : The results were summarized as follows ; 1. TFD suppressed APP, AChE, GFAP mRNA in PC-12 cell treated by $A{\beta}$. 2. TFD suppressed $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ mRNA in THP-l cell treated by LPS 3.. TFD suppressed AChE activity in cell lysate of PC-12 cell treated by $A{\beta}$. 4. TFD increased glucose and decreased AChE significantly in the serum of the memory deficit mice induced by scopolamine. 5. TFD group showed significantly inhibitory effect on the scopolamine-induced impairment of learning and memory in the experiment of Morris water maze. Conclusion : According to the above results, it is suggested that TFD might be usefully applied for prevention and treatment of Alzheimer's disease.

• Journal of Oriental Neuropsychiatry
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• v.16 no.1
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• pp.81-96
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• 2005

This experiment was designed to investigate the effect of Dichroa febrifuga(DIF) on the Alzheimer’s disease. The effects of DIF extract on $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ mRNA of THP-1 cell treated by $A{\beta}$ plus LPS and amyloid precursor proteins(APP), acetylcholinesterase(AChE), glial fibrillary acidic protein(GFAP) mRNA of PC-12 cell treated by $A{\beta}$ plus $rIL-1{\beta}$ and AChE activity of PC-12 cell lysate treated by $A{\beta}$ plus $rIL-1{\beta}$ and behavior of memory deficit mice induced by scopolamine and mice glucose, uric acid, AChE activity of memory deficit rats induced by scopolamine were investigated, respectively. The results were summarized as follows ; 1. DIF extract suppressed APP, AChE, GFAP mRNA in PC-12 cell treated by $A{\beta}$. 2. DIF extract suppressed $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ mRNA in THP-1 cell treated by LPS. 3. DIF extract suppressed AChE activity in cell lysate of PC-12 cell treated by $A{\beta}$. 4. DIF extract increased glucose, decreased uric acid and AChE significantly in the serum of the memory deficit rats induced by scopolamine. 5. DIF extract group showed significantly inhibitory effect on the memory deficit of mice induced by scopolamine in the experiment of Morris water maze. According to the above results, it is suggested that DIF extract might be usefully applied for prevention and treatment of Alzheimer’s disease and memory deficit.

• Journal of Oriental Neuropsychiatry
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• v.16 no.1
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• pp.67-80
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• 2005

This experiment was designed to investigate the effect of Rheum palmatum(RHP) on the Alzheimer's disease. The effects of RHP extract on amyloid precursor proteins(APP), acetylcholinesterase(AChE), glial fibrillary acidic protein(GFAP) mRNA of PC-12 cell treated by $A{\beta}\;and\;IL-1{\beta},\;IL-6,\;TNF-{\alpha}$ mRNA of THP-1 cell treated by LPS and AChE activity of PC-12 cell lysate treated by $A {\beta}$and behavior of memory deficit rats induced by scopolamine and mice glucose, uric acid, AChE activity of memory deficit rats induced by scopolamine were investigated, respectively. The results were summarized as follows ; 1. RHP extract suppressed APP, AChE, GFAP mRNA in PC-12 cell treated by $A{\beta} $. 2. RHP extract suppressed $IL-1{\beta} $, IL-6 $TNF-{\alpha}$ mRNA in THP-1 cell treated by LPS. 3. RHP extract suppressed AChE activity in cell lysate of PC-12 cell treated by $A{\beta}$. 4. HP extract increased glucose, decreased uric acid and AChE significantly in the serum of the memory deficit rats induced by scopolamine. 5. RHP extract group showed significantly inhibitory effect on the memory deficit of mice induced by scopolamine in the experiment of Morris water maze. According to the above results, it is suggested that RHP extract might be usefully applied for prevention and treatment of Alzheimer’s disease and memory deficit symptom.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.1
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• pp.43-51
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• 2006

This experiment was designed to investigate the effect of Amomum villosum(AMV) on the Alzheimer's disease. The effects of AMV extract on amyloid precursor proteins(APP), acetylcholinesterase(AChE), glial fibrillary acidic protein(GFAP) mRNA of PC-12 cell line treated by amyloid $\beta$ protein($A{\beta}$) : IL-$1{\beta}$, IL-6, TNF-$\alpha$ mRNA of THP-1 cell line treated by lipopolysaccharide(LPS) : AChE activity of PC-12 cell lysate treated by $A{\beta}$ : serum glucose, uric acid, AChE activity of memory deficit rats induced by scopolamine : behavior of memory deficit mice induced by scopolamine were investigated, respectively. AMV extract suppressed APP, AChE, GFAP mRNA in PC-12 cell treated by $A{\beta}$ : IL-$1{\beta}$, IL-6, TNF-$\alpha$ mRNA in THP-1 cell treated by LPS , AChE activity in cell lysate of PC-12 cell treated by $A{\beta}$. AMV extract increased glucose, decreased uric acid and AChE significantly in the serum of the memory deficit rats induced by scopolamine. AMV extract group showed significantly inhibitory effect on the memory deficit of mice induced by scopolamine in the experiment of Morris water maze. According to the above results, it is suggested that AMV extract might be usefully applied for prevention and treatment of Alzheimer's disease.

• Biomolecules & Therapeutics
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• v.11 no.2
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• pp.112-118
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• 2003

1-Methylated $\beta$-carbolines (harmaline and harmalol) and antioxidants (N-acetylcysteine and ascorbate) reduced the loss of cell viability in differentiated PC 12 cells treated with 5 mM glutamate. $\beta$-Carbolines prevented the glutamate-induced decrease in mitochondrial membrane potential, cytochrome c release and caspase-3 activation in PC 12 cells. $\beta$-Carbolines reduced the formation of reactive oxygen species and depletion of glutathione due to glutamate in PC12 cells. $\beta$-Carbolines revealed a scavenging action on hydrogen peroxide and reduced the iron and EDTA-mediated degradation of 2-deoxy-D-ribose. The results suggest that I-methylated $\beta$-carbolines attenuate the cytotoxic effect of glutamate on PC12 cells by reducing the alteration of mitochondrial membrane permeability that seems to be mediated by oxidative stress.

• The Journal of Korean Medicine
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• v.23 no.1
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• pp.50-60
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• 2002

Objectives: Sunghyangjunggisan (SHJS) is a commonly prescribed drug with a wide neuropharmacological spectrum. The water extracts of SHJS were found to be protective against neurotoxicity elicited by deprivation of serum and glucose. Methods: The morphological examination and Hoechst staining of nucleus also clearly showed that the extracts attenuated the cell shrinkage, membrane blebbing, representing typical neuronal apoptotic phenomena and nucleosome-sized fragmentation under the microscope in PC 12 rat pheochromocytoma cells. Results: Activation of protein kinase A (PKA) with dibutyl-cAMP and forskolin also protected during glucose deprivation, although it was not additive with the effect provided by phorbol ester. Interestingly, treatment with the protein kinase A inhibitor, KT5720, was not neuroprotective in the presence of SHJS. Electrophoretic mobility shift assays were used to characterize the neuroprotective binding of nuclear proteins to consensus sequences for AP-l, nuclear factor kappa B ($NF-{\kappa}B$) after glucose deprivation. When PC 12 cells are induced to undergo apoptosis by serum deprivation, AP-l and $NF-{\kappa}B$ DNA binding activity transiently increases to a slight degree. This stimulation is blocked by the water extracts of SHJS. The site of action of the drugs appeared to involve specific inhibition of AP-1 and nuclear factor kB binding activity. Conclusions: Taken together, these results suggested the possibility that the extracts of SHJS might provide a neurotrophic-like activity in PC 12 cells.