• Journal of Life Science
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• v.22 no.5
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• pp.657-664
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• 2012

The aim of this study is to screen a therapeutic agent with a cognitive function. The inhibitory effect of $Curcuma$ $longa$ hot water extract (CLWE) on the angiotension-converting enzyme and acetylcholinesterase derived from rabbit lungs and neural cells (PC12), as well as its antioxidant effect, was investigated in this study. Thus, for the first time, the direct scavenging effect of CLWE on DPPH radicals, superoxide anions, hydroxyl radicals, lipid peroxidation, reducing power, and the protective effect of DNA oxidation related to oxidative stress was evaluated in vitro. In addition, it was observed that CLWE especially exhibited a scavenging effect on reducing power and superoxide anions in this study. CLWE showed a protective effect on DNA oxidation produced by hydroxyl radicals. Furthermore, CLWE inhibited the activity of angiotensin-converting enzymes above 0.25%. Additionally, the extract inhibited oxidative stress and inducible nitric oxide in neuronal cells. Therefore, these results demonstrated that CLWE has antioxidant activity and neuronal cell protective effects, suggesting that it may have great potential as a natural source for human health.

• The Journal of Korean Medicine
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• v.26 no.4
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• pp.74-86
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• 2005

Background: There are increasing neuro-degenerative disorders with aging. Paeoniae Radix(PR) possesses various pharmacological effects such as sedative, analgesic, anti-inflammatory, anti-stress and neuro-protective actions. Also antiaging and anti-cancer effects of PR were reported. Our purpose was to investigate whether PR is useful on the treatment of Parkinson's disease, one of the neuro-degenerative disorders. Objective: We investigated whether Paeonia Radix possesses a protective effect against 1-methyl-4 phenylpyridine(MPP+)-induced cytotoxicity in neuronal cells. Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay, flow cytometry, DNA fragmentation assay, reverse transcription-polymerase chain reaction(RT-PCR), and Western blotting were performed on SK-N-MC neuroblastoma cells. Results: Cells treated with MPP+ exhibited several apoptotic features, while cells pre-treated with Paeonia Radix prior to MPP+ exposure showed s decrease in the occurrence of apoptotic features. Conclusions: These results suggest that Paeonia Radix may exert a protective effect against MPP+-induced apoptosis in SK-N-MC neuroblastoma cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.6
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• pp.1095-1101
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• 2011

Scutellariae Radix has been used as a traditional medicine for anti-oxidant, anti-inflammatory, anti-allergic function. But most study methods were restricted to in vitro and in vivo. Therefore to perform for clinical trials further for a new natural drug development is necessary and this study will be used as a basis for it. The studies selected from domestic academic database included the following key words; '황금', '黃芩', 'skullcap', 'Scutellariae Radix', 'scutellaria baicalensis' and considered were those published from 1990 to July, 2011. All 1080 studies were found to include the keywords related to the study subjects either in their title of contents or abstracts. and 298 studies were finally selected as subjects for this study. 243 studies among 293 studies were published between 2000 to 2011. Classification was proceeded according to study subjects as followed; anti-Inflammatory effect and antiallergic and antihistamin effect(66), antibacterial and antivirus effect(61), antioxidant effect(51), neuronal cell apoptosis and neuronal cell protective effect(22), liver cell protective effect(20). According to method type of study, 194 studies practicing in vitro, 60 studies practicing in vivo, 37 studies practicing in both. and 5 studies on documentary records. Most study methods were restricted in vitro and in vivo. For developmenting of function of anti-inflammatory effect and antiallergic, antihistamin effect & atopic dermatitis effect, antibacterial and antivirus effect, antioxidant effect, case report on various fields and multicenter clinical trials is necessary.

• Journal of Nutrition and Health
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• v.48 no.5
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• pp.451-456
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• 2015

Purpose: Neuronal apoptotic events induced by aging and hypoxic/ischemic conditions is an important risk factor in neurodegenerative diseases such as ischemia stroke and Alzheimer's disease. The peel of Citrus sunki Hort. ex Tanaka has long been used as a traditional medicine, based on multiple biological activities including anti-oxidant, anti-inflammation, and anti-obesity. In the current study, we examined the actions of fermented C. sunki peel extract against cobalt chloride ($CoCl_2$)-mediated hypoxic death in human neuroblastoma SH-SY5Y cells. Methods: Cell viability was measured by trypan blue exclusion. Expression of apoptosis related proteins and release of cytochrome c were detected by western blot. Production of intracellular reactive oxygen species (ROS) and apoptotic morphology were examined using 2',7'-dichlorofluorescin diacetate (DCF-DA) and 4',6-diamidino-2-phenylindole (DAPI) staining. Results: Exposure to $CoCl_2$, a well-known mimetic agent of hypoxic/ischemic condition, resulted in neuronal cell death via caspase-3 dependent pathway. Extract of fermented C. sunki peel significantly rescued the $CoCl_2$-induced neuronal toxicity with the cell viability and appearance of apoptotic morphology. Cytoprotection with fermented C. sunki peel extract was associated with a decrease in activities of caspase-3 and cleavage of poly (ADP ribose) polymerase (PARP). In addition, increase in the intracellular ROS and release of cytochrome c from mitochondria to the cytosol were inhibited by treatment with extract of fermented C. sunki peel. Conclusion: Based on these data, fermented C. sunki peel extract might have a protective effect against $CoCl_2$-induced neuronal injury partly through generation of ROS and effectors involved in mitochondrial mediated apoptosis.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.6
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• pp.333-338
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• 2011

Black ginseng (BG) has been widely used as herbal treatment for improving physiological function. In order to investigate the neuroprotective action of this herbal medicine, we examined the influence of BG on the learning and memory of rats using the Morris water maze, and we studied the effects of BG on the central cholinergic system and neural nitric oxide synthesis in the hippocampus of rats with neuronal and cognitive impairment. After middle cerebral artery occlusion was applied for 2h, the rats were administered BG (100 or 400 $mgkg^{-1}$, p.o.) daily for 2 weeks, followed by training and performance of the Morris water maze test. The rats with ischemic insults showed impaired learning and memory on the tasks. Treatment with BG produced improvement in the escape latency to find the platform. Further, the BG groups showed a reduced loss of cholinergic immunoreactivity and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d)-positive neurons in the hippocampus compared to that of the ISC group. These results demonstrated that BG has a protective effect against ischemia-induced neuronal and cognitive impairment. Our results suggest that BG might be useful for the treatment of vascular dementia.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.4
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• pp.265-271
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• 2009

Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice ($iNOS^{-1-}$) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.

• Archives of Pharmacal Research
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• v.25 no.3
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• pp.349-356
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• 2002

The present study was performed to examine the effect of fangchinoline, a bis- benzylisoquinoline alkaloid, which exhibits the characteristics of a $Ca^{2+}$ channel blocker, on cyanide-induced neurotoxicity using cultured rat cerebellar granule neurons. NaCN produced a concentration-dependent reduction of cell viability, which was blocked by MK-801, an N-methyl-D-aspartate (NMDA) receptor antagonist, verapamil, L-type$Ca^{2+}$channel blocker, and L-NAME, a nitric oxide synthase inhibitor. Pretreatment with fangchinoline over a concentration range of 0.1 to 10 $\mu$M significantly decreased the NaCN-induced neuronal cell death, glutamate release into medium, and elevation of $[Ca^{2+}]_i$ and oxidants generation. These results suggest that fangchinoline may mitigate the harmful effects of cyanide-induced neuronal cell death by interfering with $[Ca^{2+}]_i$influx, due to its function as a $Ca^{2+}$ channel blocker, and then by inhibiting glutamate release and oxidants generation.

• Journal of Ginseng Research
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• v.43 no.4
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• pp.606-617
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• 2019

Background: The Panax ginseng berry extract (GBE) is well known to have an antidiabetic effect. The aim of this study is to evaluate and investigate the protective effect of ultrasonication-processed P. ginseng berry extract (UGBE) compared with GBE on liver fibrosis induced by mild bile duct ligation (MBDL) model in rats. After ultrasonication process, the composition ratio of ginsenoside in GBE was changed. The component ratio of ginsenosides Rh1, Rh4, Rg2, Rg3, Rk1, Rk3, and F4 in the extract was elevated. Methods: In this study, the protective effect of the newly developed UGBE was evaluated on hepatotoxicity and neuronal damage in MBDL model. Silymarin (150 mg/kg) was used for positive control. UGBE (100 mg/kg, 250 mg/kg, 500 mg/kg), GBE (250 mg/kg), and silymarin (150 mg/kg) were orally administered for 6 weeks after MBDL surgery. Results: The MBDL surgery induced severe hepatotoxicity that leads to liver inflammation in rats. Also, the serum ammonia level was increased by MBDL surgery. However, the liver dysfunction of MBDL surgery-operated rats was attenuated by UGBE treatment via myeloid differentiation factor 88-dependent Toll-like receptor 4 signaling pathways. Conclusion: UGBE has a protective effect on liver fibrosis induced by MBDL in rats through inhibition of the TLR4 signaling pathway in liver.

• Journal of Mushroom
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• v.16 no.3
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• pp.213-217
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• 2018

This study was carried out to identify medicinal mushrooms with protective effects against oxidative stress in PC12 neuronal cell line, followed by evaluation of their antioxidant property. Extracts of medicinal mushrooms, including Ganoderma lucidum extract (GLE), antler-shaped Ganoderma lingzhi extract (AGLE), Hericium erinaceus extract (HEE), and Sanghuangporus baumii extract (SBE), were screened for cytotoxicity using MTT assay. None of the extracts up to $10{\mu}g/ml$ concentration affected cell viability. These extracts were further checked for their protective effect against oxidative stress-induced reactive oxygen species (ROS) production. Exposure to $50{\mu}M$ $H_2O_2$ induced ROS generation in PC12 cells, which was inhibited only by treatment with AGLE. In addition, inhibition of $H_2O_2-induced$ ROS generation by AGLE was found to be in a dose-dependent manner (2.5, 5, and $10{\mu}g/ml$). Microscopic examination of DCF fluorescence for detection of ROS showed a similar pattern. Further, antioxidant activity of AGLE was determined by ABTS radical cation assay, and its $IC_{50}$ was found to be $46.90{\pm}0.31{\mu}g/ml$. Taken together, these results suggest that AGLE may help to alleviate oxidative stress in PC12 neuronal cells.

• Journal of Korean Neurosurgical Society
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• v.38 no.6
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• pp.456-464
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• 2005

Objective : The authors investigated whether rotenone induces cellular death also in non-dopaminergic neurons and high concentration of potassium ion can show protective effect for non-dopaminergic neuron in case of rotenone-induced cytotoxicity. Methods : Neuro 2A cells was treated with rotenone, and their survival as well as cell death mechanism was estimated using 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium[MTT] assay, Lactate dehydrogenase[LDH] release assay, fluorescence microscopy, and agarose gel electrophoresis. The changes in rotenone-treated cells was also studied after co-treatment of 50mM KCl. And the protective effect of KCl was evaluated by mitochondrial membrane potential assay and compared with the effects of various antioxidants. Results : Neuro 2A cells treated with rotenone underwent apoptotic death showing chromosome condensation and fragmentation as well as DNA laddering. Co-incubation of neuro 2A cells with 50mM KCl prevented it from the cytotoxicity induced by rotenone. Intracellular accumulation of reactive oxygen species[ROS] resulting by rotenone were significantly reduced by 50mM KCl. Potassium exhibited significantly similar potency compared to the antioxidants. Conclusion : The present findings showed that potassium attenuated rotenone-induced cytotoxicity, intracellular accumulation of ROS, and fragmentation of DNA in Neuro 2A cells. These findings suggest the therapeutic potential of potassium ion in neuronal apoptosis, but the practical application of high concentration of potassium ion remains to be settled.