Peoniflorin attentuates Aβ(1–42)-mediated neurotoxicity by regulating calcium homeostasis and ameliorating oxidative stress in hippocampus of rats

Zhong, Shuzhi; Ge, Qing-Hua; Li, Qiao; Qu, Rong; Ma, Shengming

doi:10.1016/j.jns.2009.01.027

Cited by 100 publications

(70 citation statements)

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“…This leads to reduced ATP formation and induction of opening of the permeability transition pore, release of cytochrome c and activation of caspase. It has been shown that Aβ peptide triggers the activation of caspase-3, which eventually results in neuronal apoptosis (26).…”

Section: Introductionmentioning

confidence: 99%

The effect of intracerebroventricular injection of beta amyloid peptide (1-42) on caspase-3 activity, lipid peroxidation, nitric oxide and nos expression in young adult and aged rat brain

Çetin

Yazıhan²,

Dinçer³

et al. 2012

Turkish Neurosurgery

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AIm: Intracerebroventricular (icv) administration of beta amyloid peptide (Aβ) in rats can be used to model certain aspects of Alzheimer disease (AD).The purpose of this study was to examine the effects of intracerebroventricular Aβ (1-42) peptide injection on caspase-3 activity and expression of nNOS and iNOS, malondialdehyde (MDA), glutathione (GSH) and NOx in the hippocampus, temporal cortex and parietal cortex. mAterIAl and methOds: Groups were defined as 1) young adult control, 2) Aβ (1-42) injected young adult, 3) aged control and 4) Aβ (1-42) injected aged group. Stereotaxic surgery was performed. Aβ (1-42) peptide (5μg/1μl, in each icv) was administered bilateral intracerebroventricularly as a single injection.results: Caspase-3 activity significantly increased in Aβ (1-42) injected aged rats when compared with young adult rats. Aβ (1-42) significantly increased lipid peroxidation in both young adult and aged rats. There was an increase in nNOS expression in the temporal cortex of Aβ (1-42) injected aged rats. COnClusIOn:The most significant increase was seen in hippocampus in caspase-3 levels of the Aged-Aβ 1-42 group. nNOS expression in the hippocampus of aged rats was increased compared to young adult rats. However, nNOX expression in the hippocampus of Aβ (1-42) injected aged rats decreased significantly.KeywOrds: Beta amyloid, Caspase 3 activity, Lipid peroxidation, Nitric oxide, Nitric oxide synthase, Hippocampus, Aging ÖZ AmAÇ: Literatür bulguları, oksidatif stres ve kaspaz aktivitesinin amiolid beta peptid (Aβ)'in meydana getirdiği Alzheimer Hastalığı(AH) nörotoksisitesinde ve yaşlanmada rolü olduğunu göstermektedir. İntraserebroventrikuler (icv) Aβ peptid uygulamaları sıçanlarda AH'nı taklit etmek için kullanılmaktadır. Bu çalışmanın amacı, icv Aβ (1-42) peptid uygulamasının 3-4 aylık genç erişkin ve 22-24 aylık yaşlı sıçanların hipokampus, temporal korteks ve parietal kortekslerinde kaspaz 3 aktivitesi, nNOS ve iNOS ekspresyonu, MDA,GSH ve NO düzeylerine olan etkilerini araştırmaktır. yÖntem ve GereÇler: Gruplar: 1) Genç erişkin kontrol, 2) icv Aβ (1-42) enjekte edilen genç erişkin, 3) Yaşlı kontrol 4) icv Aβ (1-42) enjekte edilen yaşlı grup. Stereotaksik cerrahi uygulanarak her bir serebral ventrikül içerisine 5µg/1µl Aβ(1-42) peptid tek bir kez enjekte edildi. Aβ (1-42) uygulamasından 72 saat sonra sıçanlar dekapite edilerek beyinleri hızla buz üzerinde çıkarıldı.BulGulAr: Aβ(1-42) enjekte edilen yaşlı sıçanlarda genç erişkinlere göre kaspaz 3 aktivitesi anlamlı olarak yüksek bulundu. Aβ(1-42) enjekte edilen hem genç erişkin hem de yaşlı sıçanların temporal ve parietal kortekslerinde MDA düzeyleri anlamlı düzeyde artış gösterdi. nNOS ekspresyonu yaşlı kontrol grubunda genç erişkin kontrol gruba göre hipokampuste yüksek olarak bulundu. sOnuÇ: Yine hipokampuste Aβ(1-42) uygulamasından sonra yaşlı grupta yaşlı kontrol grubuna göre nNOS ekspresyonunda azalma bulundu. Temporal kortekste ise nNOS ekspresyonu Aβ(1-42) uygulamasından sonra yaşlı grupta artmış bulundu. iNOS ekspresyonu ise hiç...

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Section: Introductionmentioning

confidence: 99%

The effect of intracerebroventricular injection of beta amyloid peptide (1-42) on caspase-3 activity, lipid peroxidation, nitric oxide and nos expression in young adult and aged rat brain

Çetin

Yazıhan²,

Dinçer³

et al. 2012

Turkish Neurosurgery

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“…It has numerous pharmacological effects including anti-inflammatory, anti-allergy, hepatoprotective and neuromuscular blocking, among others (13)(14)(15)(16)(17). Our previous investigation revealed that paeoniflorin inhibits NF-κB activation and enhances 5-fluorouracil (5-FU)-induced apoptosis in the human gastric carcinoma cell line, SGC790 (18).…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin modulates multidrug resistance of a human gastric cancer cell line via the inhibition of NF-κB activation

Liu

2011

Mol Med Report

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Abstract.Research into the evasion of drug resistance and adverse effects is highly significant and urgent in the clinic. Therefore, accumulating studies have focused on the development of novel target-specific molecules related to drug resistance, and the establishment of rational therapeutic approaches. Currently, studies have shown that NF-κB activation may play an essential role in the development of chemotherapy resistance in carcinoma cells. Paeoniflorin, a principal bioactive component of the root of Paeonia lactiflora Pall., has been reported to exhibit various pharmacological effects. In the present study, we reported for the first time that paeoniflorin at non-toxic concentrations may effectively modulate multidrug resistance (MDR) of the human gastric cancer cell line SGC7901/vincristine (VCR) via the inhibition of NF-κB activation and, at least partly, by subsequently downregulating its target genes MDR1,

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“…Jialei Li, Department of Internal Neurology, Wuxi People's Hospital, Wuxi, Jiangsu Province, China, phone: +86 13912489660, fax: (00) 86-(0) 510-85520770, e-mail: lijialei00@gmail.com might exert beneficial action for the treatment of AD [25]. However, the molecular mechanisms by which PF exerts its neuroprotective effect against β-amyloid-induced toxicity are still unclear.…”

Section: Communicating Authormentioning

confidence: 99%

“…All cell culture reagents were purchased from Gibco (Grand Island, NY, USA). Aβ [25][26][27][28][29][30][31][32][33][34][35] , 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and rhodamine 123 (Rh123) were purchased from Sigma-Aldrich (St. Louis, Mo, USA). Annexin V-FITC and PI double staining kit were purchased from PharMingen (San Diego, CA, USA).…”

Section: Materials and Chemicalsmentioning

confidence: 99%

Original article Paeoniflorin attenuates Aβ 25-35 -induced neurotoxicity in PC12 cells by preventing mitochondrial dysfunction

Li¹,

Ji²,

Zhang³

et al. 2014

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Peoniflorin attentuates Aβ(1–42)-mediated neurotoxicity by regulating calcium homeostasis and ameliorating oxidative stress in hippocampus of rats

Cited by 100 publications

References 50 publications

The effect of intracerebroventricular injection of beta amyloid peptide (1-42) on caspase-3 activity, lipid peroxidation, nitric oxide and nos expression in young adult and aged rat brain

The effect of intracerebroventricular injection of beta amyloid peptide (1-42) on caspase-3 activity, lipid peroxidation, nitric oxide and nos expression in young adult and aged rat brain

Paeoniflorin modulates multidrug resistance of a human gastric cancer cell line via the inhibition of NF-κB activation

Original article Paeoniflorin attenuates Aβ 25-35 -induced neurotoxicity in PC12 cells by preventing mitochondrial dysfunction

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