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 56 publications

(29 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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

View full text Add to dashboard Cite

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.

show abstract

Section: Introductionmentioning

confidence: 99%

Berberine: Pathways to protect neurons

Lin

Zhang

2018

Phytotherapy Research

View full text Add to dashboard Cite

show abstract

“…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

View full text Add to dashboard Cite

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.

show abstract

“…Akt contains serine/threonine protein kinase and, following phosphorylation, Akt phosphorylates numerous intercellular substrate proteins and regulates their activities (23,24). Therefore, Akt is involved in regulating a number of intercellular signal pathways, promoting cell survival and proliferation, preventing cellular apoptosis and regulating glycometabolism and protein synthesis (25)(26)(27). bFGF, a polypeptide with various biological activities, functions in an identical manner as a neurotrophic factor (28)(29)(30) and promotes the survival of nerve cells via numerous conduction pathways.…”

Section: Discussionmentioning

confidence: 99%

Akt regulates β-catenin in a rat model of focal cerebral ischemia-reperfusion injury

Xue-song

Liu

2014

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. The present study aimed to investigate the effects of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway on the Wnt/β-catenin signaling pathway in rats with focal cerebral ischemia-reperfusion injury. A total of 96 rat focal cerebral ischemia-reperfusion models, established according to a modified version of Longa's method, were randomly divided into four groups: Sham-operated (S), cerebral ischemia-reperfusion injury (I), cerebral ischemia-reperfusion + basic fibroblast growth factor (bFGF) post-processing and, finally, cerebral ischemia-reperfusion + bFGF post-processing + PI3K inhibitor LY294002 (LY). Each group consisted of 24 rats and each group was divided into four subgroups according to the indicated reperfusion times of 12, 24, 48 and 72 h. The morphological changes of the cortical tissue and the cellular apoptosis were determined using hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase dUTP nick end labeling method, respectively. The expression levels of phosphorylated (p-)Akt, glycogen synthase kinase-3β (GSK-3β) mRNA and β-catenin in the cortical tissue were detected at different time-points. The number of apoptotic cells and the expression levels of p-Akt, GSK-3β mRNA and β-catenin in the I and LY groups were significantly higher compared with those in the S group (P<0.05). In the bFGF group, the number of apoptotic cells and the mRNA expression levels of GSK-3β were significantly decreased, whereas the expression levels of p-Akt and β-catenin were significantly increased compared with those in the I and LY groups (P<0.05). In cerebral ischemia-reperfusion injury, the PI3K/Akt signaling pathway regulated β-catenin, the main member of the Wnt signaling pathway, via GSK-3β, providing information to assist in further investigation of the mechanism of β-catenin in ischemia-reperfusion injury.

show abstract

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 56 publications

References 35 publications

Berberine: Pathways to protect neurons

Berberine: Pathways to protect neurons

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

Akt regulates β-catenin in a rat model of focal cerebral ischemia-reperfusion injury

Contact Info

Product

Resources

About