• 대한본초학회지
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• 제23권3호
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• pp.19-25
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• 2008

Objectives : This study was performed to evaluate the neuroprotective effect of water extracts from Thujae Semen(TSW) in PC12 cells. Methods : We performed 2,2-diphenyl-2-picrylhydrazyl(DPPH) radical scavenging assay, 2,2-azinobis- (3-ethyl-benzothiazoline-6-sulfonic acid(ABTS) cation scavenging assay, and determination of total polyphenolic content to examine the antioxidant effects of TSW. We also carried out 3-(4,5- dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay(MTT), reactve oxygen species(ROS) assay, and nitric oxide(NO) assay to examine neuroprotective effects against 6-hydroxydopamine(6-OHDA) in PC12 cells. Results : TSW showed $IC_{50}$ values of 404.3 and 219.9 ${\mu}g/mL$ in DPPH and in ABTS assays, respectively. TSW showed 9.74 ${\mu}g/mL$ of total polyphenol contents. TSW incresed cell viability in a dose dependent manner and it showed protective effect against 6-OHDA neurotoxicity at the concentration of 25-200 ${\mu}g/mL$. Moreover, it recovered 6-OHDA induced cell death at the same concentrations. The extract showed a dose dependent reduction of ROS and NO generation by 6-OHDA. Conclusions : We concluded that TSW has neuroprotective effect against 6-OHDA-induced toxicity in PC12 cells through ROS and NO inhibition.

• BMB Reports
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• 제56권3호
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• pp.202-207
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• 2023

We investigated the neuroprotective effects of deca nano-graphene oxide (daNGO) against reactive oxygen species (ROS) and inflammation in the human neuroblastoma cell line SH-SY5Y and in the 6-hydroxydopamine (6-OHDA) induced Parkinsonian rat model. An MTT assay was performed to measure cell viability in vitro in the presence of 6-OHDA and/or daNGO. The intracellular ROS level was quantified using 2',7'-dichlorofluorescein diacetate. daNGO showed neuroprotective effects against 6-OHDA-induced toxicity and also displayed ROS scavenging properties. We then tested the protective effects of daNGO against 6-OHDA induced toxicity in a rat model. Stepping tests showed that the akinesia symptoms were improved in the daNGO group compared to the control group. Moreover, in an apomorphine-induced rotation test, the number of net contralateral rotations was decreased in the daNGO group compared to the control group. By immunofluorescent staining, the animals in the daNGO group had more tyrosine hydroxylase-positive cells than the controls. By anti-Iba1 staining, 6-OHDA induced microglial activation showed a significantly decrease in the daNGO group, indicating that the neuroprotective effects of graphene resulted from anti-inflammation. In conclusion, nano-graphene oxide has neuroprotective effects against the neurotoxin induced by 6-OHDA on dopaminergic neurons.

• 한국한의학연구원논문집
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• 제5권1호
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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.

• Journal of Ginseng Research
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• 제21권1호
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• pp.61-67
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• 1997

The present study examined the characteristics of behavior Induced by dopamine agonists following treatment with 6-hydroxydopamine(6-OHDA) unilaterally into left striatum in rats. 6-OHDA was administered at doses of 8,16 and 24 $\mu\textrm{g}$/$\mu\textrm{l}$(in 0.1% ascorbic acid) into dopaminergic neurons in left striatum of 7 weeks old rat under anesthetic. Locomotor activity was significantly decreased at 1 week following 6-OHDA-administration in 7 weeks old rats. The contralateral circling behavior was induced by apomorphine(5 mg/kg, i.v.) after 1 week following 6-OHDA(24$\mu\textrm{g}$/$\mu\textrm{l}$) treatment, and was further increased by repeated administration of apomorphine at 2, 3 and 4 weeks. The contralateral circling behavior was also induced by lisuride and 1-dopa in a dose dependent manner, but not by SK & F 82526 in 7 weeks old rats treated with 6-OHDA. The contralateral circling behavior was significantly higher in 21 weeks old rats but significantly lower In 35 weeks old rats when compared with 7 weeks old rats. The contralateral circling behavior induced by apomorphlne did not differ significantly in 7 and 35 weeks old male and female rats. These results suggest that 6-OHDA treatment into left striatum causes remarkable destrurtion of intrastriatal dopaminergic netcons leading to dopaminergic receptor supersensitivity. Thus, the contralateral circling behavior in duces by apomorphine may be used as indicator for neurodegenerative diseases.

• Journal of Korean Biological Nursing Science
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• 제22권4호
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• pp.223-231
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• 2020

Purpose: The purpose of this study was to investigate the effects of taro extract on brain resilience in in vitro Parkinson's disease model induced by 6-hydroxydopamine (6-OHDA). Methods: To induce a neuroinflammatory reaction and the in vitro Parkinson's disease model, SH-SY5Y cells were stimulated with lipopolysaccharide (LPS) and 6-OHDA, respectively. After that, cells were treated with at various concentrations (1, 5, and 10 mg/mL) of taro extract. Then nitric oxide (NO) production, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, synaptophysin (SYP) and growth associated protein (GAP)-43 messenger ribonucleic acid (mRNA) expression level were measured. Results: Taro extract significantly suppressed LPS-induced NO production. Meanwhile, iNOS and IL-6 mRNA expression decreased in a dose-dependent manner. In addition, taro increased the mRNA expression of SYP and GAP-43 mRNA. Conclusion: These findings indicate that taro played an important role in brain resilience by inhibiting neuronal cell death and promoting neurite outgrowth, synaptogenesis, and neural plasticity. The results of this study suggest that taro may contribute to the prevention of neurodegenerative disease and become a new and safe therapeutic strategy for Parkinson's disease.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.196.2-197
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• 2003

Parkinson's disease (PO) is a widespread neurodegenerative disorder. Even though PD has been studied in many aspects, it is still unknown the molecular signaling mechanisms linking reactive oxygen species (ROS) and neuronal apoptosis in PD. A better understanding of cellular mechanisms that occur in Parkinson's disease is essential for development of new therapies. In this study we investigated the signaling molecules involved in neuronal apoptosis induced by 6-hydroxydopamine (6-OHDA) in human SK-N-SH neuroblastoma cells as a model cellular system. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• 제10권6호
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• pp.309-315
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• 2006

The protective effects of baicalein, one of the flavonoids in Scutellaria baicalensis Georgi, were evaluated against 6-hydroxydopamine (6-OHDA)-induced neuronal damage in mice and cultured human neuroblastoma cells. Nigrostriatal damage was induced by stereotaxically injecting 6-OHDA into the right striatum. Baicalein was administered intraperitoneally 30 min before and 90 min after lesion induction. Animals received a further daily injection of baicalein for 3 consecutive days. Two weeks after 6-OHDA injection, contralateral rotational asymmetry was observed by apomorphine challenge in lesioned mice. Tyrosine hydroxylase (TH) immunohistochemistry revealed a significant loss of terminals in lesioned striatum and the reduction of the numbers of TH-positive cell in the ipsilateral substantia nigra (SN). In addition, the levels of dopamine (DA) and DA metabolites were reduced and lipid peroxidation was increased in lesioned striatum. However, baicalein treatment reduced apomorphine-induced rotational behavior in 6-OHDA-lesioned mice, and increased TH immunoreactivity in the striatum and SN, and DA levels in lesioned striatum. Lipid peroxidation induced by 6-OHDA was also inhibited by baicalein treatment. Furthermore, when SH-SY5Y human neuroblastoma cells were treated with baicalein, 6-OHDA-induced cytotoxicity and reactive oxygen species (ROS) production were significantly reduced. These results indicate that baicalein effectively protects 6-OHDA-induced neuronal damage through antioxidant action.

• 대한한의학회지
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• 제26권4호
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• pp.98-107
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• 2005

Objectives: Acupuncture treatment has been clinically used for functional recovery in Parkinson's disease. In the present study, we investigated the effect of acupuncture at Zusanli (ST36) on nigrostriatal dopaminergic neuronal cell death in rats. Methods: A Parkinson's disease model was induced by the unilateral injection of 6-hydroxydopamine (6-OHDA) into the striatum. Acupuncture treatment was performed at Zusanli (ST36) and at the hip, as a non-acupoint, once a day for 14 days. Two weeks after 6-0HDA injection, an apomorphine-induced rotational behavior test showed significant rotational asymmetry in rats with Parkinson's disease. Immunostaining for tyrosine hydroxylase demonstrated a dopaminergic neuronal loss in the substantia nigra and dopaminergic fiber loss in the striatum. Results: Acupuncture at the ST36 acupoint significantly inhibited rotational asymmetry in rats with Parkinson's disease, and also protected against 6-OHDA-induced nigrostriatal dopaminergic neuronal loss. These effects of acupuncture were not observed for non-acupoint acupuncture. Conclusions: The present study shows that acupuncture treatment, especially at the ST36 acupoint, can be used as a useful strategy for the treatment of Parkinson's disease.

• Nutritional Sciences
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• 제9권2호
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• pp.61-67
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• 2006

Green tea has attracted attention with respect to its potential for preventing and treating neurodegenerative disease. The neurotoxin, 6-hydroxydopamine (6-OHDA), was used to produce experimental Parkinson's disease (PD) model. The purpose of this study was to investigate the effects of green tea diet on behavioral changes, striatal dopamine content, and hepatic antioxidant parameters of PD model rats. In this study, we used male Sprague-Dawley rats weighing $200\sim220g$ and injected 6-OHDA into the right substantia nigra and medial forebrain bundle of the brain. The supply of green tea diet was started at 2 weeks before 6-OHDA lesion and continually supplied during 0, 2, and 4 weeks after 6-OHDA lesion (GT-0, GT-2, GT-4). Behavioral disturbance was measured by the stepping and d-amphetamine drug-induced rotation tests. Then, we assayed the striatal dopamine content and the hepatic malondialdehyde (MDA), hydrogen peroxide $(H_2O_2)$, and superoxide dismutase (SOD) activity. The percentage of lesioned forepaw to non-lesioned forepaw step scores was the highest in GT-4 group among all groups at both 3 and 4 weeks after 6-OHDA lesion. At 4 weeks after 6-OHDA lesion, the rotation score was the lowest in GT-2 group (p<0.05). However, increasing rate of the rotation score from 2 to 4 weeks after 6-OHDA lesion was the lowest in GT-4 group. The striatal dopamine content was not significantly different among four groups by green tea diet. The hepatic MDA level was the lowest in GT-4 group among four groups. The hepatic SOD activity was increased with the prolongation of green tea diet period These results suggest that green tea diet affects behavioral changes in rats of PD model. It seems that continuous green tea supplementation has an influence on the reduction of behavioral disturbance and the hepatic MDA level. Accordingly, continuous green tea supplementation was recommended for the prevention and treatment of PD. However, further studies are needed to investigate the mechanisms and efficacy of green tea in PD.

• Biomolecules & Therapeutics
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• 제26권2호
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• pp.175-181
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• 2018

Carbon monoxide (CO) is well-known as toxic gas and intrinsic signaling molecule such as neurotransmitter and blood vessel relaxant. Recently, it has been reported that low concentration of CO exerts therapeutic actions under various pathological conditions including liver failure, heart failure, gastric cancer, and cardiac arrest. However, little has been known about the effect of CO in neurodegenerative diseases like Parkinson's disease (PD). To test whether CO could exert a beneficial action during oxidative cell death in PD, we examined the effects of CO on 6-hydroxydopamine (6-OHDA)-induced cell death in C6 glioma cells. Treatment of CO-releasing molecule-2 (CORM-2) significantly attenuated 6-OHDA-induced apoptotic cell death in a dose-dependent manner. CORM-2 treatment decreased Bax/Bcl2 ratio and caspase-3 activity, which had been increased by 6-OHDA. CORM-2 increased phosphorylation of NF-E2-related factor 2 (Nrf2) which is a transcription factor regulating antioxidant proteins. Subsequently, CORM-2 also increased the expression of heme oxygenase-1 and superoxide dismutases (CuZnSOD and MnSOD), which were antioxidant enzymes regulated by Nrf2. These results suggest that CO released by CORM-2 treatment may have protective effects against oxidative cell death in PD through the potentiation of cellular adaptive survival responses via activation of Nrf2 and upregulation of heme oxygenase-1, leading to increasing antioxidant defense capacity.