Effect of berberine on cell cycle arrest and cell survival during cerebral ischemia and reperfusion and correlations with p53/cyclin D1 and PI3K/Akt

Chai, Yu Shuang; Hu, Jun; Fan, Lei; Wang, Yu Gang; Yuan, Zhi Yi; Lü, Xi; Wang, Xin Pei; Feng, Du; Zhang, Dong; Xing, Dong; Du, Lijun

doi:10.1016/j.ejphar.2013.02.041

Cited by 60 publications

(29 citation statements)

References 35 publications

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“…Classical or widely acknowledged pathways such as the survival and apoptosis pathways (Simoes, Frozza, Hoppe, Menezes, & Salbego, ) have already proved to be involved in vitro or in vivo model of brain ischemia and reperfusion. Others such as p53/cyclin D1 (Chai et al, ), SPHK1/S1P signaling pathway (Luo et al, ), and ERK1/2 pathway (Zhu et al, ) are shown to serve as an integral part of neuroprotection in different animal models when preconditioned with BBR.…”

Section: Introductionmentioning

confidence: 99%

Berberine: Pathways to protect neurons

Lin

Zhang

2018

Phytotherapy Research

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Berberine, an isoquinoline alkaloid, is demonstrated to have a variety of pharmacologic effects. Widely used as nonprescription drug for diarrhea, berberine has also broadened its applications in therapies of cardiovascular diseases, diabetes mellitus, tumor, and so forth. However, researches about berberine's protective effects on nervous system are still so insufficient that clinical uses cannot popularize and underlying molecules mechanisms are confused and incomplete. Well-known pathways such as Pl3K/Akt/Bcl-2 pathway, Nrf2/HO-1 pathway, and MAPK signaling pathway help berberine to protect neurons through antiapoptotic, antioxidative, and anti-inflammatory activities. New hypotheses have been raised consistently to explore more possible ways of berberine preventing nerves from injuries as attention on its neuroprotective properties is increasing. Therefore, this review is trying to analyze these mechanisms, which actually play roles in neuronal disease models such as brain ischemia, Alzheimer's disease, and experimental autoimmune encephalomyelitis. Much more understanding about how berberine mediates these pathways provides novel insights into the clinical treatment of neurological disorders.

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Section: Introductionmentioning

confidence: 99%

Berberine: Pathways to protect neurons

Lin

Zhang

2018

Phytotherapy Research

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“…They found that the 344 activation of PI3 K/Akt pathway by Berberine plays an important 345 role in its neuroprotection activity against ischemic stroke [132]. 346 Similarly, Cui et al [133] anti-apoptotic mechanism of tetrohydroBerberine [140].…”

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confidence: 99%

Berberine and neurodegeneration: A review of literature

Ahmed

Gilani

Abdollahi

et al. 2015

Pharmacological Reports

172

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The excessive production of reactive oxygen species in nervous tissues is considered one of the major risk factors of neurodegenerative diseases. During the last two decades, much attention has been paid to the antioxidant and anti-inflammatory activity of natural products and compounds isolated from natural products which are often characterized by high efficacy and low adverse effects. Berberine is an isoquinoline alkaloid, widely present in different medicinal herbs, especially in the genus Berberis. It is mainly used as antidiarrhoeal, antibacterial, antifungal, and antiprotozoal agent. However, current research has focused on its beneficial role in neurodegenerative diseases, mainly due to its powerful antioxidant effect. The therapeutic potential of Berberine in different neurodegenerative diseases such as Alzheimer, Parkinson and Huntington disease has been brought to evidence by numerous studies. However, a limited number of reviews focus on the beneficial role of Berberine against neurodegeneration. The main objective of this review is to discuss the role of oxidative stress in neurodegeneration and the potential role of antioxidant compounds, in particular Berberine which is analyzed in its chemical structure, source, bioavailability, therapeutic potential, with special attention to its mechanism of action at a molecular level.

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“…It has been found that neurons re-enter into cell cycle in neurodegenerative diseases. It has been shown that the neuroprotective effect of berberine during ischemia was mediated by decreased p53 and cyclin D1, increased phosphorylation of Bad (higher expression of p-Bad and higher ratio of p-Bad to Bad) and decreased cleavage of caspase 3 [26]. It was also found that treatment with the CDK inhibitor roscovitine decreased the expression of phosphorRb and reduced neuronal apoptosis in vitro under OGD [27].…”

Section: Discussionmentioning

confidence: 60%

Metformin Protects Neurons against Oxygen-Glucose Deprivation/Reoxygenation -Induced Injury by Down-Regulating MAD2B

Meng

Chu

Yang

et al. 2016

Cell Physiol Biochem

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Background/Aims: Metformin, the common medication for type II diabetes, has protective effects on cerebral ischemia. However, the molecular mechanisms are far from clear. Mitotic arrest deficient 2-like protein 2 (MAD2B), an inhibitor of the anaphase-promoting complex (APC), is widely expressed in hippocampal and cortical neurons and plays an important role in mediating high glucose-induced neurotoxicity. The present study investigated whether metformin modifies the expression of MAD2B and to exert its neuroprotective effects in primary cultured cortical neurons during oxygen-glucose deprivation/reoxygenation (OGD/R), a widely used in vitro model of ischemia/reperfusion. Methods: Primary cortical neurons were cultured, deprived of oxygen-glucose for 1 h, and then recovered with oxygen-glucose for 12 h and 24 h. Cell viability was measured by detecting the levels of lactate dehydrogenase (LDH) in culture medium. The levels of MAD2B, cyclin B and p-histone 3 were measured by Western blot. Results: Cell viability of neurons was reduced under oxygen-glucose deprivation/reoxygenation (OGD/R). The expression of MAD2B was increased under OGD/R. The levels of cyclin B1, which is a substrate of APC, were also increased. Moreover, OGD/R up-regulated the phosphorylation levels of histone 3, which is the induction of aberrant re-entry of post-mitotic neurons. However, pretreatment of neurons with metformin alleviated OGD/R-induced injury. Metformin further decreased the expression of MAD2B, cyclin B1 and phosphorylation levels of histone 3. Conclusion: Metformin exerts its neuroprotective effect through regulating the expression of MAD2B in neurons under OGD/R.

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Effect of berberine on cell cycle arrest and cell survival during cerebral ischemia and reperfusion and correlations with p53/cyclin D1 and PI3K/Akt

Cited by 60 publications

References 35 publications

Berberine: Pathways to protect neurons

Berberine: Pathways to protect neurons

Berberine and neurodegeneration: A review of literature

Metformin Protects Neurons against Oxygen-Glucose Deprivation/Reoxygenation -Induced Injury by Down-Regulating MAD2B

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