The neuroprotective mechanism of puerarin in the treatment of acute spinal ischemia–reperfusion injury is linked to cyclin-dependent kinase 5

Tian, Feng; Xu, Lihui; Wang, Bin; Tian, Lijie; Ji, Xianglu

doi:10.1016/j.neulet.2014.09.049

Cited by 17 publications

(16 citation statements)

References 26 publications

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“…Indeed, several Chinese traditional herbal medicines have been discovered to be neuroprotective and can inhibit the activity of Cdk5/p25. For example, (I) Tanshinone IIA and Fuzhisan inhibit the neurotoxicity induced by β-amyloid, which involves in calpain and the p35/Cdk5 pathway [132,133] and (II) puerarin in the treatment of acute spinal ischemia-reperfusion injury is linked to Cdk5 [134]. However, the accurate mechanism of these medicines and whether they are effective to cure AD remain obscure.…”

Section: Cdk5: a Potential Therapeutic Target For Admentioning

confidence: 99%

The Role of Cdk5 in Alzheimer’s Disease

et al. 2015

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Alzheimer's disease (AD) is known as the most fatal chronic neurodegenerative disease in adults along with progressive loss of memory and other cognitive function disorders. Cyclin-dependent kinase 5 (Cdk5), a unique member of the cyclin-dependent kinases (Cdks), is reported to intimately associate with the process of the pathogenesis of AD. Cdk5 is of vital importance in the development of CNS and neuron movements such as neuronal migration and differentiation, synaptic functions, and memory consolidation. However, when neurons suffer from pathological stimuli, Cdk5 activity becomes hyperactive and causes aberrant hyperphosphorylation of various substrates of Cdk5 like amyloid precursor protein (APP), tau and neurofilament, resulting in neurodegenerative diseases like AD. Deregulation of Cdk5 contributes to an array of pathological events in AD, ranging from formation of senile plaques and neurofibrillary tangles, synaptic damage, mitochondrial dysfunction to cell cycle reactivation as well as neuronal cell apoptosis. More importantly, an inhibition of Cdk5 activity with inhibitors such as RNA inference (RNAi) could protect from memory decline and neuronal cell loss through suppressing β-amyloid (Aβ)-induced neurotoxicity and tauopathies. This review will briefly describe the above-mentioned possible roles of Cdk5 in the physiological and pathological mechanisms of AD, further discussing recent advances and challenges in Cdk5 as a therapeutic target.

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Section: Cdk5: a Potential Therapeutic Target For Admentioning

confidence: 99%

The Role of Cdk5 in Alzheimer’s Disease

et al. 2015

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“…PR has been demonstrated to exert a broad spectrum of pharmacological effects, such as vasodilation, 21 cardioprotection, 22 neuroprotection, 23 antioxidant, 24 anticancer, 25 anti-inflammation, 26 and inhibition of diabetic ocular complications. 27 Recently, the neuroprotective effects of PR have been reported in some experimental models, such as those of spinal cord injury 28,29 and cerebral ischemia injury. 30,31 The antiapoptotic capacity of PR was reported in RGC damage through the inhibition of the JNK/p38 MAPK pathway.…”

mentioning

confidence: 99%

Therapeutic Effects of Puerarin Against Anterior Ischemic Optic Neuropathy Through Antiapoptotic and Anti-Inflammatory Actions

Wen²,

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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“…Puerarin, a primary component of Kudzu root, has recently been reported to be an active neuroprotective agent in the models of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Amyotrophic lateral sclerosis (ALS) [ 26 , 27 ]. Puerarin has also been widely used in the clinical treatment of retinal degenerative diseases in China for decades due to its neuroprotective effect.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Puerarin on Glutamate-Induced Cytotoxicity in Differentiated Y-79 Cells via Inhibition of ROS Generation and Ca2+ Influx

Wang¹,

Zhu²,

Zhang³

et al. 2016

IJMS

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Glutamate toxicity is estimated to be the key cause of photoreceptor degeneration in the pathogenesis of retinal degenerative diseases. Oxidative stress and Ca2+ influx induced by glutamate are responsible for the apoptosis process of photoreceptor degeneration. Puerarin, a primary component of Kudzu root, has been widely used in the clinical treatment of retinal degenerative diseases in China for decades; however, the detailed molecular mechanism underlying this effect remains unclear. In this study, the neuroprotective effect of puerarin against glutamate-induced cytotoxicity in the differentiated Y-79 cells was first investigated through cytotoxicity assay. Then the molecular mechanism of this effect regarding anti-oxidative stress and Ca2+ hemostasis was further explored with indirect immunofluorescence, flow cytometric analysis and western blot analysis. Our study showed that glutamate induced cell viability loss, excessive reactive oxygen species (ROS) generation, calcium overload and up-regulated cell apoptosis in differentiated Y-79 cells, which effect was significantly attenuated with the pre-treatment of puerarin in a dose-dependent manner. Furthermore, our data indicated that the neuroprotective effect of puerarin was potentially mediated through the inhibition of glutamate-induced activation of mitochondrial-dependent signaling pathway and calmodulin-dependent protein kinase II (CaMKII)-dependent apoptosis signal-regulating kinase 1(ASK-1)/c-Jun N-terminal kinase (JNK)/p38 signaling pathway. The present study supports the notion that puerarin may be a promising neuroprotective agent in the prevention of retinal degenerative diseases.

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The neuroprotective mechanism of puerarin in the treatment of acute spinal ischemia–reperfusion injury is linked to cyclin-dependent kinase 5

Cited by 17 publications

References 26 publications

The Role of Cdk5 in Alzheimer’s Disease

The Role of Cdk5 in Alzheimer’s Disease

Therapeutic Effects of Puerarin Against Anterior Ischemic Optic Neuropathy Through Antiapoptotic and Anti-Inflammatory Actions

Neuroprotective Effect of Puerarin on Glutamate-Induced Cytotoxicity in Differentiated Y-79 Cells via Inhibition of ROS Generation and Ca2+ Influx

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