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Dangguijakyak-san, a medicinal herbal formula, protects dopaminergic neurons from 6-hydroxydopamine-induced neurotoxicity. | LitMetric

Dangguijakyak-san, a medicinal herbal formula, protects dopaminergic neurons from 6-hydroxydopamine-induced neurotoxicity.

J Ethnopharmacol

Department of Oriental Gynecology, College of Oriental Medicine, Kyung Hee University, #1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.

Published: January 2011

AI Article Synopsis

  • The study investigates the neuroprotective effects of the herbal formula Dangguijakyak-san (DJS) against damage to dopaminergic neurons caused by 6-hydroxydopamine (6-OHDA), which is relevant in treating gynecologic disorders and neurological symptoms.
  • Researchers tested DJS on neuroblastoma cells and primary dopaminergic cells, assessing cell viability and analyzing anti-oxidant activities as well as mitochondrial functions.
  • Results showed that DJS significantly protected cells from 6-OHDA toxicity, reducing harmful reactive oxygen species (ROS), preventing mitochondrial instability, and inhibiting pathways leading to cell death, indicating its potential as a neuroprotective agent.

Article Abstract

Aim Of The Study: Dangguijakyak-san (DJS) is a multi-herbal formula that has long been widely used in traditional Oriental medicine to treat gynecologic disorders, including neurological symptoms. Recent clinical and experimental studies have reported aging and anti-neurodegenerative effects of DJS. In this study, we evaluated the neuroprotective effects of DJS on dopaminergic (DA) neurons damaged by 6-hydroxydopamine (6-OHDA).

Materials And Methods: To evaluate the protective effects of DJS, we analyzed viability in SH-SY5Y neuroblastoma cells and tyrosine hydroxylase (TH) staining in primary DA cells. To explore the possible mechanism(s) of neuroprotection, we assessed anti-oxidant activity by measuring reactive oxygen species (ROS) and glutathione (GSH) levels. To determine mitochondria-mediated apoptotic activity, we examined mitochondrial membrane potential, cytochrome c release, and caspase-3 activation.

Results: DJS at 0.05-5 μg/mL significantly protected SH-SY5Y cells from 6-OHDA toxicity, dose-dependently, and attenuated 6-OHDA damage in primary DA cells. DJS reduced 6-OHDA-induced intracellular ROS production and GSH depletion and inhibited mitochondrial membrane instability, cytosolic cytochrome c release, and caspase-3 activation.

Conclusions: These results demonstrate that DJS has neuroprotective effects in DA neurons against 6-OHDA-induced toxicity through anti-oxidant and anti-mitochondrial-mediated apoptotic activities.

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Source
http://dx.doi.org/10.1016/j.jep.2010.11.017DOI Listing

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