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7. Neuroprotective effect of chunghyuldan from amyloid beta oligomer induced neuroinflammation in vitro and in vivo

Author

Kim, Hyo Geun, Kim, Ji-Young, Whang, Wei-Wan, and Oh, Myung Sook

Subjects
Amyloid beta-protein -- Physiological aspects, Medicinal plants -- Physiological aspects, Biological sciences
Abstract

Microglia-mediated inflammation is a major pathological mechanism contributing to Alzheimer's disease (AD), and has been proposed as a potential therapeutic target. Chunghyuldan (CHD; Qingxue-dan in Chinese and Daio-Orengedokuto in Japanese) possesses wide-ranging biological effects, including anti-hyperlipidemic, anti-stroke, anti-inflammatory, and antioxidant activities that could affect neurological functions. In this study, we examined the effects of CHD in in-vitro and in- vivo models of AD induced by the oligomeric form of amyloid-beta (Aβ oligomer), which acts directly on microglia- mediated neuroinflammation to result in neuronal damage and cognitive impairment. CHD at 0.1-100 µg-[mL.sup.-1] significantly protected PC12 cells and rat primary hippocampal cells from Aβ [oligomer.sub.1-42] toxicity. In addition, CHD at 1-10 µg x [mL.sup.-1] inhibited Aβ [oligomer.sub.1-42] induced production of nitric oxide, tumor necrosis factor-α, and interleukin-1β in microglial cells. In an in-vivo AD model, administration of CHD [(50 µg x (kg body mass).sup.-1] , for 5 days, per oral) inhibited the activation of astrocytes and microglia in the dentate gyrus and neuronal damage in the CA1 of the ipsilateral hippocampus. Moreover, CHD ameliorated cognitive impairment induced by Aβ [oligomer.sub.1-42] toxicity. These results demonstrate the neuroprotective effects of CHD through inhibition of microglia-mediated neuroinflammation in in-vitro and in-vivo AD-like models induced by Aβ [oligomer.sub.1-42] toxicity. Key words: Chunghyuldan, oligomeric form of amyloid-beta, Alzheimer's disease, neuroinflammation. L'inflammation dependante de la microglie constitue un mecanisme pathologique important qui contribue a la maladie d'Alzheimer (MA), et elle a ete proposee comme cible therapeutique potentielle. Le Chunghyuldan (CHD, Qingxue- dan en Chinois et Daio-Orengedokuto en Japonais) possede un large spectre d'effets biologiques, y compris des activites antihyperlipemiques, anti-AVC, anti-inflammatoires et anti-oxydantes qui pourraient affecter les fonctions neurologiques. Dans cette etude, les auteurs ont examine les effets du CHD dans des modeles in vitro et in vivo de MA induite par la forme oligomere du beta-amyloide (Ap), qui agit directement sur la neuro-inflammation dependante de la microglie et resulte en dommages neuronaux et en deficience cognitive. Le CHD de 0,1 a 100 g-[mL.sup.-1] protegeait significativement les cellules PC12 et les cellules primaires d'hippocampe de rat de la toxicite de l'oligomere [Aβ.sub.1-42]. De plus, le CHD de 1 a 10 µg x [mL.sup.-1] inhibait dans les cellules de la microglie, la production d'oxyde nitrique, du facteur necrosant des tumeurs-a et d'interleukine-1β induite par l'oligomere [Aβ.sub.1-42]. Dans un modele in vivo de MA, l'administration de CHD [(50 µg x (kg de masse corporelle).sup.-1] , 5 jours, per oral) inhibait l'activation des astrocytes et de la microglie dans le giron dente, ainsi que le dommage neuronal dans l'aire CA1 de l'hippocampe ipsilateral. En outre, le CHD ameliorait les deficiences cognitives induites par la toxicite de l'oligomere [Aβ.sub.1-42]. Ces resultats demontrent les effets neuro-protecteurs du CHD a travers l'inhibition de la neuro-inflammation dependante de la microglie dans des modeles de MA induits in vitro et in vivo par la toxicite de l'oligomere [Aβ.sub.1-42]. [Traduit par la Redaction] Mots-cles: Chunghyuldan, forme oligomere du p-amyloide, maladie d'Alzheimer, neuro-inflammation., Introduction Alzheimer's disease (AD) accounts for 60%-70% of dementias and affects Widespread inflammatory changes are observed in the AD brain, particularly at the amyloid deposits rich in activated microglia (Akiyama [...]

Published
2014
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49. An Optimized Combination of Ginger and Peony Root Effectively Inhibits Amyloid-β Accumulation and Amyloid-β-Mediated Pathology in AβPP/PS1 Double-Transgenic Mice.

Author

Soonmin Lim, Jin Gyu Choi, Minho Moon, Hyo Geun Kim, Wonil Lee, Hyoung-rok Bak, Hachang Sung, Chi Hye Park, Sun Yeou Kim, Myung Sook Oh, Lim, Soonmin, Choi, Jin Gyu, Moon, Minho, Kim, Hyo Geun, Lee, Wonil, Bak, Hyoung-Rok, Sung, Hachang, Park, Chi Hye, Kim, Sun Yeou, and Oh, Myung Sook

Subjects
AMYLOID, ALZHEIMER'S disease, HERBAL medicine, LABORATORY mice, INFLAMMATION, DIAGNOSIS, BIOTHERAPY, ANALYSIS of variance, ANIMAL experimentation, BIOLOGICAL models, CYTOSKELETAL proteins, DOSE-effect relationship in pharmacology, GINGER, MEMBRANE proteins, MICE, GENETIC mutation, OXIDOREDUCTASES, PEPTIDES, PLANTS, PROTEIN precursors
Abstract

The progressive aggregation of amyloid-β protein (Aβ) into senile plaques is a major pathological factor of Alzheimer's disease (AD) and is believed to result in memory impairment. We aimed to investigate the effect of an optimized combination of ginger and peony root (OCGP), a standardized herbal mixture of ginger and peony root, on Aβ accumulation and memory impairment in amyloid-β protein precursor (AβPP)/presenilin 1 (PS1) double-transgenic mice. In an in vitro thioflavin T fluorescence assay, 100 μg/ml OCGP inhibited Aβ accumulation to the same extent as did 10 μM curcumin. Furthermore, AβPP/PS1 double-transgenic mice treated with OCGP (50 or 100 mg/kg/day given orally for 14 weeks) exhibited reduced Aβ plaque accumulation in the hippocampus and lower levels of glial fibrillary acid protein and cyclooxygease-2 expression compared with vehicle-treated controls. These results suggest that OCGP may prevent memory impairment in AD by inhibiting Aβ accumulation and inflammation in the brain. [ABSTRACT FROM AUTHOR]

Published
2016
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