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Anti-parkinsonian effect of Cyperi Rhizoma via inhibition of neuroinflammatory action

향부자(香附子)의 염증 억제 작용을 통한 항파킨슨 효과

  • Kim, Hyo Geun (Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University) ;
  • Sim, Yeomoon (Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University) ;
  • Oh, Myung Sook (Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University)
  • 김효근 (경희대학교 약학대학 한약학과) ;
  • 심여문 (경희대학교 약학대학 한약학과) ;
  • 오명숙 (경희대학교 약학대학 한약학과)
  • Received : 2013.08.15
  • Accepted : 2013.09.13
  • Published : 2013.09.30

Abstract

Objectives : The aim of this study was to investigate the neuroprotective effects and mechanisms of Cyperi Rhizoma extracts (CRE) using in vitro and in vivo models of Parkinson's disease (PD). Methods : We evaluated the neuroprotective effect of CRE against 1-methyl-4-phenylpyridinium (MPP+) toxicity using tyrosine hydroxylase immunohistochemistry (IHC) in primary rat mesencephalic dopaminergic neurons. In addition, the effect of CRE was evaluated in mice PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). For evaluations, C57bl/6 mice were orally treated with CRE 50 mg/kg for 5 days and were injected intraperitoneally with MPTP (20 mg/kg) at 2 h intervals on the last day. To identify the CRE affects on MPTP-induced neuronal loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) and striatum of mice, the behavioral tests and IHC analysis were carried out. Also, we conducted nitric oxide (NO) and tumor necrosis factor-alpha (TNF-${\alpha}$) assay in dopaminergic neurons and IHC using glial markers in SNpc of mice to assess the anti-inflammation effects. Results : In primary mesencephalic culture system, CRE protected dopaminergic cells against $10{\mu}M$ MPP+-induced toxicity at 0.2 and $1.0{\mu}g/mL$. In the behavior tests, CRE treated group showed improved motor deteriorations than those in the MPTP only treated group. CRE significantly protected striatal dopaminergic damage from MPTP-induced neurotoxicity in mice. Moreover, CRE inhibited productions of NO and TNF-${\alpha}$ in dopaminergic culture system and activation of astrocyte and microglia in SNpc of the mice. Conclusion : We concluded that CRE shows anti-parkinsonian effect by protecting dopaminergic neurons against MPP+/MPTP toxicities through anti-inflammatory actions.

Keywords

References

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