• Korean Journal of Pharmacognosy
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• v.30 no.1
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• pp.79-83
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• 1999

The effects of coralyne, a protoberberine isoquinoline compound, on dopamine biosynthesis in PC12 cells were investigated. Coralyne decreased the dopamine content dose-dependently $(46.3%\;inhibition\;at\;20\;{\mu}M\;for\;24 hr).$ Dopamine content was lowered at 6 hr and reached minimal level at 24 hr after exposure to coralyne at $20\;{\mu}M.$ The decreased dopamine level was maintained up to 48 hr and recovered to the control level at about 72 hr. Tyrosine hydroxylase, the rate-limiting enzyme in the catecholamine biosynthesis, was also inhibited at $20\;{\mu}M\;of\;coralyne$ by 16.1% relative to control. These results suggest that the inhibition of tyrosine hydroxylase by coralyne with a single treatment might be partially contributed to the decrease in dopamine content in PC12 cells.

• Korean Journal of Pharmacognosy
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• v.26 no.1
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• pp.57-61
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• 1995

MeOH extracts of eight herbal medicines were investigated for the effects on catecholamine biosynthesis and tyrosine hydroxylase (TH) activity in PC12 cells. Among them, the MeOH extracts of Polygalae Radix and Rehmaniae Radix showed 32 and 22% inhibition on the dopamine biosynthesis, respectively at a concentration of $40{\mu}g/ml$ medium. But, the TH activity was reduced by the treatment of Polygalae Radix. These results suggest that Polygalae Radix has an inhibitory effect on the catecholamine biosynthesis by the reduction of TH activity in PC12 cells.

• Korean Journal of Pharmacognosy
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• v.36 no.2 s.141
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• pp.151-157
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• 2005

This research was performed to investigate the protective effect of Chungpesagan-tang (CST) from hypoxia/reperfusion induced-PC12 cell damage. To elucidate the mechanism of the protective effect of CST, cell viability, changes in activities of superoxide dismutase, glutathione peroxidase, catalase, caspase 3 and the production of malondialdehyde were observed after treating PC12 cells with CST which was metabolized by rat liver homogenate. Pretreatment of CST with liver homogenate appeared to increase its protective effect against hypoxia/reperfusion insult. The result showed that CST exhibited the highest protective effect against hypoxia/reperfusion at the dose of $1\;{\mu}g/ml$ in PC12 cells, probably by recovering the redox enzyme activities and MDA to control level.

• YAKHAK HOEJI
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• v.42 no.2
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• pp.170-174
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• 1998

The effects of bulbocapnine, an aporphine isoquinoline alkaloid, on dopamine content in PC12 cells were investigated. Bulbocapnine decreased the dopamine content dose-dependentl y (39.2% inhibition at 2O${\mu}$M for 24 hr). The $IC_{50}$ value of bulbocapnine was 22.7${\mu}$M. Dopamine content was lowered at 6 hr after exposure to bulbocapnine. And then, the decreased dopamine level was almost maintained at 36 hr and recovered to the control level at about 60 hr. Tyrosine hydroxylase, the rate limiting enzyme in the catecholamine blosynthetic pathway, was also inhibited at 20${\mu}$M of bulbocapnine by 23.1% relative to control. We, therefore, hypothesized that the inhibition of tyrosine hydroxylase by bulbocapnine with a single treatment might be partially contributed to the decrease in dopamine content in PC12 cells.

• YAKHAK HOEJI
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• v.49 no.1
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• pp.97-102
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• 2005

The protective effect of Yangguksanwha-tang (YST) against hypoxia-reperfusion insult was investigated in PC12 cells. To elucidate the mechanism of the protective effect of YST, cell viability, the changes in activities of superoxide dismutase, glutathione peroxidase, catalase, caspase 3 and the production of malondialdehyde were observed after treating PC12 cells with YST which was metabolized by rat liver homogenate. Pretreatment of YST with liver homogenate appeared to increase its protective effect against hypoxia-reperfusion insult. The result showed that YST had the highest protective effect against hypoxia/reperfusion at the dose of $2\;{\mu}g/ml$ in PC12 cells, probably by recovering the redox enzyme activities and MDA to control level.

• YAKHAK HOEJI
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• v.54 no.5
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• pp.323-327
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• 2010

Translationally controlled tumor protein (TCTP) activates basophils to release histamine and causes chronic inflammation. It was also reported that TCTP significantly reduced in brain of Alzheimer's Disease and Down Syndrome as compared to normal person, suggesting that TCTP might be involved in cognitive function. We wondered whether TCTP could act as a general inducer in neurotransmitters release in brain. We, therefore, investigated the role of TCTP in PC12 cell line which expressed neuronal properties. We found that TCTP could activate JNK, and the activity was inhibited by pretreatment of dicoumarol, a JNK inhibitor. However, TCTP could not activate ERK that has known to be involved in neurotransmitter release. These suggest TCTP did not participate in neurotransmitter release from PC12 cells, and TCTP might not be a general inducer in neurotransmitter release.

• Korean Journal of Oriental Medicine
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• v.5 no.1
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• pp.119-131
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• 1999

The effect of herbal medicine on 1-methyl-4-phenylpyridinium ion $(MPP^+)$ and 6-hydroxydopamine (6-OHDA) mediated neurotoxicity was studied in the rat phaeochromocytoma cell line PC12. The present study was designed to test the hypothesis that herbal medicine can protect cells from neurotoxiciy caused by $MPP^+$ and 6-OHDA. Exposure of PC12 cells to 0.2 mM $MPP^+$ and $50\;{\mu}M$ 6-OHDA for 24h resulted in a 50% cell death with respect to the control cells. $MPP^+$ induced cell death was reduced by Yollyounggobondan (延齡固本丹), Sagunjatang (四君子湯), Palmihwan (八味丸), and Palmultang (八物湯)(P<0.05). However, herbal medicines did not protect cells from degeneration caused by the 6-OHDA. Yollyounggobondan, Yungmijihwangwon (六味地黃元), Palmihwan, and Samultang (四物湯) were effective in protecting against $MPP^+$-induced ATP loss in PC12 cells (P<0.05). Yollyounggobondan and Palmultang were effect in neurite protection against 6-OHDA treatment in differentiated PC12 cells with NGF.

• YAKHAK HOEJI
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• v.50 no.2
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• pp.105-110
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• 2006

The effects of tributyltin acetate (TBTA), one of the endocrine-disrupting organotin compounds, on dopamine biosynthesis in PC12 cells were investigated. Treatment of PC12 cells with TBTA at $0.05\sim0.25{\mu}M$ significantly decreased the intracellular dopamine content in a concentration-dependent manner ($IC_{50}$ value, $0.17{\mu}M$). Under these conditions, tyrosine hydroxylase (TH) activity and TH mRNA level were also decreased by $0.1{\mu}M$ TBTA at 24 h, and recovered there-after. In addition, treatment with L-DOPA at 20 and $50 {\mu}M$ increased the intracellular dopamine content in PC12 cells and the increase in dopamine content by L-DOPA was significantly abolished by TBTA at $0.1\sim0.2{\mu}M$. These results indicate that TBTA at $0.1\sim0.2{\mu}M$ causes the decrease in the basal dopamine content and abolishes the increase in dopamine content in L-DOPA-treated cells in part by the inhibition of TH gene expression and activity.

• Biomedical Science Letters
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• v.15 no.4
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• pp.287-293
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• 2009

Phospholipase D (PLD) is an enzyme hydrolyzing phosphatidylcholine to phosphatidic acid (PA) and choline. We investigated the involvement of PLD1 in the uptake of norepinephrine (NE) in PC12 cells, pheochromocytoma cells. NE uptake was specific in PC12 cells because nomifensine, a specific blocker of NE transporter, blocked NE uptake. Inhibition of PLD function in PC12 cells by the treatment of butanol suppressed the NE uptake. In contrast, overexpression of PLD1 in PC12 cells increased NE uptake efficiently. These results suggest that PLD activity is involved in NE uptake. We explored the action mechanism of PLD in NE uptake. PA phosphatase inhibitor, propranolol, blocks the formation of PKC activator diacylglycerol from PA. Propranolol treatment to PC12 cells blocked dramatically the uptake of NE. Specific PKC inhibitors, GF109203X and Ro31-8220, blocked NE uptake. Taken together, we suggest for the first time that PLD1 activity is involved in NE uptake via the activation of PKC.

• Natural Product Sciences
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• v.20 no.4
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• pp.296-300
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• 2014

The present study investigated the effects of (-)-sesamin on dopamine biosynthesis in PC12 cells. Treatment with (-)-sesamin (25 and $50{\mu}M$) increased intracellular dopamine levels and enhanced L-DOPA-induced increase in dopamine levels in PC12 cells. (-)-Sesamin (25 and $50{\mu}M$) also induced the phosphorylation of cyclic AMP-dependent kinase A (PKA), cyclic AMP-response element binding protein (CREB) and tyrosine hydroxylase (TH) in PC12 cells. These results suggest that (-)-sesamin induces dopamine biosynthesis via the PKA-CREB-TH pathways in PC12 cells. (-)-Sesamin needs to be studied further to serve as an adjuvant phytonutrient in neurodegenerative disease.