• Title/Summary/Keyword: Dopaminergic

Search Result 339, Processing Time 0.026 seconds

Neuroprotective Effect of Insamyangyung-tang (인삼양영탕(人蔘養營湯)의 산화적 stress에 대한 뇌세포 보호효과)

  • Kim, Seung-Hyun;Lee, Chang-Hoon;Lee, Jin-Moo;Cho, Jung-Hoon;Jang, Jun-Bock;Lee, Kyung-Sub
    • The Journal of Korean Obstetrics and Gynecology
    • /
    • v.22 no.1
    • /
    • pp.1-14
    • /
    • 2009
  • Purpose: Oxidative stress was thought to play a critical role in neurodegenerative disease. Many in vivo and in vitro reports explained the possible pathway of human aging. But in therapeutic aspects, there was no clear answers to prevent aging associated with neural diseases. In this study, we investigated the antioxidant and neuroprotective effects of the Insamyangyung-tang (IYT). Methods: To estimate the antioxidant effects, we carried out 1.1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging assay, 2,2'-azinobis-(3- ethylbenzothiazoline-6- sulfonic acid (ABTS) radical cation decolorization assay, and measurement of total polyphenolic content. To evaluate neuroprotective effect of IYT in vitro. We performed thiazolyl blue tetrazolium bromide (MTT) assay, reactive oxygen species (ROS) creation in SH-SY5Y. Tyrosine hydroxylase (TH) immunocytochemistry, nitric oxide (NO) assay, and TNF-${\alpha}$ assay in primary rat mesencephalic dopaminergic neurons. Results: The $IC_{50}$ values were $571.6{\mu}g/m{\ell}$ and $202.3{\mu}g/m{\ell}$ in DPPH and ABTS assay respectively. Total polyphenolic content was 1.05%. In SH-SY5Y culture, IYT significantly increased the decreased cell viability by 6-OHDA at the concentrations of $10{\mu}g/m{\ell}$ in pre-treatment group, $10-100{\mu}g/m{\ell}$ in post-treatment group, and $100{\mu}g/m{\ell}$ in co-treatment group. The production of ROS induced by 6-OHDA was significantly inhibited in IYT treated group. In mesencephalic dopaminergic cell culture, the IYT group reduced the dopaminergic cell loss against 6-OHDA toxicity and the production of No and TNF-${\alpha}$ at the concentration of $0.2{\mu}g/m{\ell}$. Conclusion: These results showed that IYT has antioxidant and neuroprotectctive effects in the dopaminergic cells through decreasing the production of ROS, NO and TNF-${\alpha}$ which can cause many neurodegenerative changes in brain cell.

Neuroprotective Effect of Yukul-tang against the Oxidative Stress (육울탕(六鬱湯)의 산화적 스트레스에 대한 뇌세포 보호효과)

  • Jung, Sun-Hyung;Lee, Jin-Moo;Lee, Chang-Hoon;Cho, Jung-Hoon;Jang, Jun-Bock;Lee, Kyung-Sub
    • The Journal of Korean Obstetrics and Gynecology
    • /
    • v.22 no.1
    • /
    • pp.15-30
    • /
    • 2009
  • Purpose: In this rapidly aging society, the research and development of traditional oriental medicine treatment is one of the critical factors to protect the increasing neuro-degenerative disorders. In this study, we wanted to verify the effect of Yukul-tang (YUT) on neuro-degenerative disease model by assessing the antioxidant and anti-inflammation effects. Methods: To assess the antioxidant effects of YUT, we carried out DPPH radical and ABTS radical scavenging assays and determined the total polyphenolic contents in YUT. To evaluate the neuro-protective effects of YUT, we performed the MTT and ROS assays and TH immunohistochemistry, NO and TNF-${\alpha}$ assays in SH-SY5Y or mesencephalic dopaminergic neurons damaged by 6-OHDA. Results: The treatment of YUT showed eliminating effects on DPPH radical and ABTS radical. it showed deterring effects on ROS, NO and TNF-${\alpha}$ and protecting effects on TH-positive cell in SH-SY5Y cells or mesencephalic dopaminergic neurons. Especially in the case of the treatment of YUT with 0.2ug/mL + 6-OHDA 10uM, the protective effect on dopaminergic neurons was most outstanding. Conclusion: In this study, we have demonstrated that YUT has an antioxidant effect and a neuro-protective effect on neuro-degenerative disease model caused by neurotoxin such as 6-OHDA. The results of our present study suggest that YUT can be useful agent to prevent and to treat neuro-degenerative diseases.

Neuroprotective Effects of Cervi Cornu in MPP+ Treated SH-SY5Y Cells (MPP+로 유도된 신경 독성에 대한 녹각의 보호 효과)

  • Yeo, Sujung
    • Korean Journal of Acupuncture
    • /
    • v.37 no.2
    • /
    • pp.97-103
    • /
    • 2020
  • Objectives : Parkinson's disease, a progressive neurodegenerative disease, is caused by the loss of dopaminergic neurons in the substantia nigra. There is no clear treatment or remedy for Parkinson's disease; therefore, the development of novel therapies related to anti-inflammatory and antioxidant effects is required. This study was performed to evaluate the neuroprotective effect of water extracts from Cervi Cornu (CC) in dopaminergic cells. Methods : We studied effects of CC on apoptosis, cell death and inflammation in SH-SY5Y neuroblastoma cells treated by methylpyridinium ion (MPP+). SH-SY5Y cell line was treated with CC for 24 hours and then 500 μM MPP+ for 18 hours. Results : Cervi Cornu treatment inhibited the decrease in tyrosine hydroxylase (TH) expression and decreased the activation of inflammatory factors mitochondrial cytochrome C oxidase (COX2) and inducible NO synthase (iNOS) against MPP+ neurotoxicity. Apoptosis factors BCL2 associated X, apoptosis regulator (BAX) levels were decreased and B-Cell CLL/Lymphoma 2 (BCL2) levels were increased. Conclusions : These results suggest that CC treatment had neuroprotective effects in the SH-SY5Y neuroblastoma cells against toxicity induced by MPP+. The results suggest new possibilities of CC for the treatment of Parkinson's disease.

Changes in Behavior and the Effect of Chronic-methamphetamine Following Lesions of the Nucleus Accumbens Septi in Rats (측좌핵(側坐核)(Nucleus Accumbens Septi) 파괴가 Methamphetamine의 작용에 미치는 영향)

  • Lee Soon-Chul
    • The Korean Journal of Pharmacology
    • /
    • v.20 no.1 s.34
    • /
    • pp.33-39
    • /
    • 1984
  • The present study was undertaken to elucidate the chracteristics in behavioral changes of chronic doses of methamphetamine on open-field activity in rats. On the other hand, the nucleus accumbens septi(NAB), one of the major areas containing mesolimbic dopaminergic terminals, has been considered to be an important site of action for dopaminergic agonists. Therefore, it also designed to investigated influence of NAB lesions. on behavioral effects of chronic-methamphetamine. Caudal and rostral areas of NAB(cr-NAB) were lesioned by applying DC of 3.0 mA for 15 sec., simultaneously. The results were as follows: 1) The rats exhibited hyperactivity after chronic administration of methamphetamine 2) The cr-NAB-lesioned rats showed a significant increase in locomotor activity only at 2 days after NAB lesions 3) Methamphetamine-induced hyperactivity was significantly decreased in the NAB-lesioned rats, and stereotyped behavior was induced instead by the drug. 4) Dopamine content of striatum was significantly decreased and serotonin content of olfactory bulb was significantly increased in NAB-lesioned rats. These results suggest that NAB plays an important role in locomotor activity and methamphetamine-induced hyperactivity.

  • PDF

Xylazine-induced depression and its antagonism by α-adrenergic blocking agents (Xylazine의 진정효과와 α-adrenergic 수용체 봉쇄약물의 길항효과)

  • Kim, Chung-hui;Hah, Dae-sik;Kim, Yang-mi;Kim, Jong-shu
    • Korean Journal of Veterinary Research
    • /
    • v.33 no.1
    • /
    • pp.71-80
    • /
    • 1993
  • The central nervous system depressant effect of xylazine and xylazine-ketamine was studied in chicken and mice. Intraperitoneal injection of xylazine(1~30 mg/kg) and xylazine(1~30 mg/kg)-ketamine(100 mg/kg) induced a loss of the righting reflex in chicken and mice, respectively. These effects of xylazine were dose-dependent. The results obtained were as follows; 1. The effect of xylazine-induced depression was antagonized by adrenergic antagonists having ${\alpha}_2$-blocking activity(yohimbine, tolazoline, piperoxan and phentolamine). 2. Yohimbine was most effective in the reduction of the CNS depression by xylazine. 3. Phenoxybenzamine and prazosin did not reduced CNS depression by xylazine in both species. 4. Labetalol (${\alpha}_1$, ${\beta}_1$-adrenergic antagonist) and propranolol(${\beta}$-adrenergic blocking agent) were not effective in reducing xylazine induced depression. 5. Cholinergic blocking agents (atropine and mecamylamine), a dopaminergic antagonist (Haloperidol), a histamine $H_1$-antagonist(chlorpheniramine), a histamine $H_2$-antagonist(cimetidine), a serotonergic-histamine $H_1$ antagonist(cyproheptadine) were not effective in reducing xylazine-induced depression. 6. Xylazine-induced depression is mediated by ${\alpha}_2$-adrenergic receptors and appears not to be involved in cholinergic, dopaminergic, serotonergic or histaminergic pathways.

  • PDF