Neuroprotective effects of puerarin against beta-amyloid-induced neurotoxicity in PC12 cells via a PI3K-dependent signaling pathway

Xing, Guihua; Dong, Miaoxian; Li, Xiaoming; Zou, Yu; Fan, Li; Wang, Xiaoli; Cai, Defu; Li, Chengchong; Zhou, Li; Liu, Jicheng; Niu, Yingcai

doi:10.1016/j.brainresbull.2011.03.024

Cited by 85 publications

(50 citation statements)

References 48 publications

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“…Moreover, we found that expression of cytochrome c and Puma were reduced, alongside with the restoration of Bcl-2/Bax and Bcl-xL/Bax ratio in the presence of biochanin A, which led to a decrease in the apoptotic rate. These data demonstrate that mitochondria are involved in the protective effect of biochanin A against Aβ [25][26][27][28][29][30][31][32][33][34][35] and that this drug attenuated Aβ 25-35 -induced PC12 cell injury and apoptosis by preventing mitochondrial dysfunction. Thus, biochanin A might raise a possibility as a potential therapeutic agent for Alzheimer's disease and other related neurodegenerative diseases.…”

Section: Introductionmentioning

confidence: 74%

“…The β-amyloid (Aβ) protein is the major component of senile plaques and has a causal role in the development and progression of AD [3]. Its peptide fragment chain Aβ [25][26][27][28][29][30][31][32][33][34][35] is the most toxic derivative, and has been universally applied in the research of AD [4]. Although the actual mechanism associated with Aβ-induced toxicity remains elusive, some studies have demonstrated evidence that oxidative stress and mitochondrial dysfunction play a role in Aβ-mediated neuronal cytotoxicity [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective Effects of Biochanin A against β-Amyloid-Induced Neurotoxicity in PC12 Cells via a Mitochondrial-Dependent Apoptosis Pathway

Tan

Kim

2016

Molecules

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Abstract:Alzheimer's disease is considered one of the major neurodegenerative diseases and is characterized by the production of β-amyloid (Aβ) proteins and progressive loss of neurons. Biochanin A, a phytoestrogen compound found mainly in Trifolium pratense, was used in the present study as a potential alternative to estrogen replacement therapy via the investigation of its neuroprotective effects against Aβ 25-35 -induced toxicity, as well as of its potential mechanisms of action in PC12 cells. Exposure of these cells to the Aβ 25-35 protein significantly increased cell viability loss and apoptosis. However, the effects induced by Aβ 25-35 were markedly reversed in the present of biochanin A. Pretreatment with biochanin A attenuated the cytotoxic effect of the Aβ 25-35 protein by decreasing viability loss, LDH release, and caspase activity in cells. Moreover, we found that expression of cytochrome c and Puma were reduced, alongside with the restoration of Bcl-2/Bax and Bcl-xL/Bax ratio in the presence of biochanin A, which led to a decrease in the apoptotic rate. These data demonstrate that mitochondria are involved in the protective effect of biochanin A against Aβ [25][26][27][28][29][30][31][32][33][34][35] and that this drug attenuated Aβ 25-35 -induced PC12 cell injury and apoptosis by preventing mitochondrial dysfunction. Thus, biochanin A might raise a possibility as a potential therapeutic agent for Alzheimer's disease and other related neurodegenerative diseases.

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Section: Introductionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Biochanin A against β-Amyloid-Induced Neurotoxicity in PC12 Cells via a Mitochondrial-Dependent Apoptosis Pathway

Tan

Kim

2016

Molecules

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“…Furthermore, we showed that puerarin could block CoCl 2 -induced hypoxic damage on b-cell function and survival, because CoCl 2 is also commonly used as a hypoxia-like inducer and the puerarin protection was mediated through upregulating the anti-oxidant Sod2 and Gpx1, and the anti-apoptotic Bcl-2, while decreasing the pro-apoptotic Bax. Puerarin has beneficial effects in various tissues, including hepatocyte, neural cells, kidney, endothelial cells, and osteoblastic cells, protecting the cell survival from a variety of damage, such as b-amyloid, lead, 1-methyl-4-phenylpyridinium iodide, cisplatin, especially oxidative stress, in which PI3K/Akt played a pivotal role (Hwang & Jeong 2008, Hwang et al 2011, Xing et al 2011, Zhang et al 2012, Zhu et al 2012. Here, in clonial MIN6 b-cells, we observed a rapid activation of Akt phosphorylation by puerarin.…”

Section: Discussionmentioning

confidence: 55%

Puerarin protects pancreatic β-cell survival via PI3K/Akt signaling pathway

Li¹,

Shangguan²,

Liu³

et al. 2014

Journal of Molecular Endocrinology

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Pancreatic b-cell loss because of apoptosis is the major cause of type 1 diabetes (T1D) and late stage T2D. Puerarin possesses anti-diabetic properties; whether it acts directly on pancreatic b-cell is not clear. This study was designed to investigate the effects of puerarin on pancreatic b-cell survival and function. Diabetes was induced in male C57BL/6 mice by a single peritoneal injection of streptozotocin (STZ). Pancreatic b-cell survival and function were assessed in diabetic mice by measuring b-cell apoptosis, b-cell mass, pancreatic insulin content, and glucose tolerance, and in cultured islets and clonial MIN6 b-cells by measuring b-cell viability and apoptosis and glucose-stimulated insulin secretion. We found that pre-treatment with puerarin decreased the incidence of STZ-induced diabetes. Puerarin increased pancreatic b-cell mass via b-cell apoptosis inhibition in diabetic mice, and increased serum insulin, whereas it decreased blood glucose levels and improved glucose tolerance. In cultured islets and MIN6 cells, puerarin protected b-cell from cobalt chloride (CoCl 2 )-induced apoptosis and restored the impaired capacity of glucose-stimulated insulin secretion. Puerarin protection of b-cell survival involved the phosphoinositide 3-kinase (PI3K) /Akt signaling pathway. In conclusion, puerarin protects pancreatic b-cell function and survival via direct effects on b-cells, and its protection of b-cell survival is mediated by the PI3K/Akt pathway. As a safe natural plant extraction, puerarin might serve as a preventive and/or therapeutic approach for diabetes.

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“…no. 15140122; all from Thermo Fisher Scientific, Inc., Waltham, MA, USA), and maintained at 37˚C in a humidified incubator in a 5% CO 2 atmosphere for 2-3 d. PC12 cells were treated with NGF (50 ng/ml) for 2 days at 37˚C to induce neuronal differentiation, and subsequently examined by a microscope (13,14). Differentiated PC12 cells were used in all experiments.…”

Section: Chemicalsmentioning

confidence: 99%

Di-Huang-Yi-Zhi herbal formula attenuates amyloid-β-induced neurotoxicity in PC12 cells

Chen

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Traditional Chinese medicine can be used for Alzheimer's disease management, such as the modern herbal formula Di-Huang-Yi-Zhi (DHYZ). In the present study, neuronal differentiated PC12 cells were used as a model to evaluate the effects of DHYZ against amyloid-β peptide 25-35 (Aβ 25-35 ) induced neurotoxicity, particularly regarding cell proliferation, apoptosis and related events. Following treatment with DHYZ, cell viability, cell membrane damage, apoptosis, mitochondrial membrane potential, cytochrome c release, caspase-3 activity and levels of reactive oxygen species in PC12 cells were detected. The results demonstrated that pretreatment with DHYZ significantly protected PC12 cells from Aβ 25-35 -induced proliferation inhibition, lactate dehydrogenase release and apoptosis, as well as upregulating mitochondrial membrane potential and downregulating cytochrome c release and caspase-3 activation. DHYZ also inhibited the Aβ 25-35 -induced reactive oxygen species generation in PC12 cells. These observations suggest that DHYZ protected PC12 cells from the Aβ-induced neurotoxicity.

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Neuroprotective effects of puerarin against beta-amyloid-induced neurotoxicity in PC12 cells via a PI3K-dependent signaling pathway

Cited by 85 publications

References 48 publications

Neuroprotective Effects of Biochanin A against β-Amyloid-Induced Neurotoxicity in PC12 Cells via a Mitochondrial-Dependent Apoptosis Pathway

Neuroprotective Effects of Biochanin A against β-Amyloid-Induced Neurotoxicity in PC12 Cells via a Mitochondrial-Dependent Apoptosis Pathway

Puerarin protects pancreatic β-cell survival via PI3K/Akt signaling pathway

Di-Huang-Yi-Zhi herbal formula attenuates amyloid-β-induced neurotoxicity in PC12 cells

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