Neuroprotective effect of nobiletin on cerebral ischemia–reperfusion injury in transient middle cerebral artery-occluded rats

Yasuda, Nodoka; Ishii, Takayuki; Oyama, Dai; Fukuta, Tatsuya; Agato, Yurika; Sato, Akihiko; Shimizu, Kosuke; Asai, Tomohiro; Asakawa, Tomohiro; Kan, Toshiyuki; Yamada, Shizuo; Ohizumi, Yasushi; Oku, Naoto

doi:10.1016/j.brainres.2014.02.007

Cited by 78 publications

(37 citation statements)

References 32 publications

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“…Hence, nobiletin mitigated nephrotoxicity of cisplatin by attenuating apoptosis in cisplatin injected rats. The anti-apoptotic effect of nobiletin has been reported in a rat model of cerebral ischemia reperfusion injury by Yasuda et al (2014). Thus, plausible mechanism underlying nobiletin's nephroprotective effect may be attributed to its anti-oxidative and anti-apoptotic effects.…”

Section: Discussionmentioning

confidence: 91%

“…Numerous studies have reported that nobiletin has many important pharmacological effects (Miyata et al, 2004;Assini et al, 2013;Lee et al, 2013;Yasuda et al, 2014). With respect to oxidative stress and apoptosis, a study by Lu et al (2010) showed that nobiletin restored glutathione and superoxide dismutase activities and diminished malondialdehyde and caspase-3 activity in PC12 cells when exposed to hydrogen peroxide.…”

Section: Introductionmentioning

confidence: 95%

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Nobiletin ameliorates cisplatin-induced acute kidney injury due to its anti-oxidant, anti-inflammatory and anti-apoptotic effects

Malik

Bhatia

Suchal

et al. 2015

Experimental and Toxicologic Pathology

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 95%

Nobiletin ameliorates cisplatin-induced acute kidney injury due to its anti-oxidant, anti-inflammatory and anti-apoptotic effects

Malik

Bhatia

Suchal

et al. 2015

Experimental and Toxicologic Pathology

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“…It has been established that inflammatory reactions are responsible for neuronal damage in cerebral ischemia, including focal and global ischemia (7,24). A number of investigations have demonstrated the critical role of inflammation after ischemia and reperfusion in stroke (7,8).…”

Section: Discussionmentioning

confidence: 99%

Pinocembrin alleviates memory impairment in transient global cerebral ischemic rats

Meng

Wang

Liu

et al. 2014

Experimental and Therapeutic Medicine

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The aim of the present study was to investigate the effect of pinocembrin on cognitive ability impairment in a rat model of transient global cerebral ischemia (TGCI). The TGCI model was established by inducing global cerebral ischemia for 20 min, followed by reperfusion for two weeks. The rats were divided into five experimental groups, including the sham group that were not subjected to ischemia, and four ischemic groups where the rats were exposed to TGCI. The sham and control TGCI groups were administered a vehicle intravenously immediately after reperfusion, while the other three groups were intravenously treated with 1, 5 and 10 mg/kg pinocembrin, respectively. In the present study, neurological scores were analyzed at 0 and 24 h after reperfusion, and the effect of pinocembrin on cognitive ability impairment in the TGCI rat model was investigated using a Morris water maze test. Neuronal loss was observed under an optical microscope with the assistance of Nissl staining. In addition, glial fibrillary acidic protein (GFAP)-positive cells were observed under an optical microscope by an immunohistochemistry assay. Pinocembrin treatment was found to alleviate the cognitive impairments, decrease the neurological scores, diminish neuronal loss in the hippocampus and reduce the number of GFAP-positive cells in the hippocampal CA1 region of the TGCI rats. Therefore, pinocembrin alleviated memory impairment in the TGCI rats.

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“…The remainder of the models listed in Table 1 are focused on the chemical lesioning of cholinergic pathways using various excitotoxins, or are models based on hypoxia and/or stroke induction (Cada, de la Torre, & Gonzalez-Lima, 2000;Nguyen et al, 2018;Yang et al, 2013;Yasuda et al, 2014).…”

Section: Wild-type Animal Models Of Dementia and Admentioning

confidence: 99%

Preclinical Models of Alzheimer's Disease: Relevance and Translational Validity

Mullane

Williams

2019

CP Pharmacology

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The only drugs currently approved for the treatment of Alzheimer's Disease (AD) are four acetylcholinesterase inhibitors and the NMDA antagonist memantine. Apart from these drugs, which have minimal to no clinical benefit, the 40‐year search for effective therapeutics to treat AD has resulted in a clinical failure rate of 100% not only for compounds that prevent brain amyloid deposition or remove existing amyloid plaques but also those acting by a variety of other putative disease‐associated mechanisms. This indicates that the preclinical data generated from current AD targets to support the selection, optimization, and translation of new chemical entities (NCEs) and biologics to clinical trials is seriously compromised. While many of these failures reflect flawed hypotheses or a lack of adequate characterization of the preclinical pharmacodynamic and pharmacokinetic (PD/PK) properties of lead NCEs—including their bioavailability and toxicity—the conceptualization, validation, and interrogation of the current animal models of AD represent key limitations. The overwhelming majority of these AD models are transgenic, based on aspects of the amyloid hypothesis and the genetics of the familial form of the disease. As a result, these generally lack construct and predictive validity for the sporadic form of the human disease. The 170 or so transgenic models, perhaps the largest number ever focused on a single disease, use rodents, mainly mice, and in addition to amyloid also address aspects of tau causality with more complex multigene models including other presumed causative factors together with amyloid. This overview discusses the current animal models of AD in the context of both the controversies surrounding the causative role of amyloid in the disease and the need to develop validated models of cognitive function/dysfunction that more appropriately reflect the phenotype(s) of human aged‐related dementias. © 2019 by John Wiley & Sons, Inc.

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Neuroprotective effect of nobiletin on cerebral ischemia–reperfusion injury in transient middle cerebral artery-occluded rats

Cited by 78 publications

References 32 publications

Nobiletin ameliorates cisplatin-induced acute kidney injury due to its anti-oxidant, anti-inflammatory and anti-apoptotic effects

Nobiletin ameliorates cisplatin-induced acute kidney injury due to its anti-oxidant, anti-inflammatory and anti-apoptotic effects

Pinocembrin alleviates memory impairment in transient global cerebral ischemic rats

Preclinical Models of Alzheimer's Disease: Relevance and Translational Validity

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