Abstract
ABSTRACT Objectives : The aim of this study was to investigate the neuroprotective ef fects 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-methy l-4-phenylpyridinium (MPP+) toxicity using tyrosine hydroxylase immunohistochemistry (IHC) in primar y rat mesencephalic dopaminergic neurons. In addition, the effect of CRE was evaluated in mice PD model indu ced 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 substanti a 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-α) 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 µM MPP+-induced toxicity at 0.2 and 1.0 µg/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 pro ductions of NO and TNF-α 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 protect ing dopaminergic neurons against MPP+/MPTP toxicities through anti-inflammatory actions.Key words : Cyperi Rhizoma, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Parkinson’s disease, Neuroinflammation
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