scholarly journals Protective effect of EGb761 against Aβ1-42 -induced SHSY5Y cells injury and blood-brain barrier disruption via regulating Akt/Nrf2 signaling pathway

2021 ◽  
Vol 20 (9) ◽  
pp. 1811-1818
Author(s):  
Liling Wang ◽  
Jianhua Mi ◽  
Yeping Song ◽  
Pengfei Wang

Purpose: Alzheimer’s disease (AD) is a common disease in the world caused by deposition in the brain parenchyma, accumulation of beta amyloid which leads to the blood brain barrier (BBB) disruption. Regardless of enough progress in the treatment of AD, the principal mechanism of BBB injury is yet not clear.Methods: In this study we examined the impact of EGb761on Aβ 1-42-induced SH-SY5Y cells in vitro  model of AD. Cell viability was assessed by using MTT assay, flow cytometry was used to check the rate of cell apoptosis, ROS generation and BBB leakage was assessed by measuring the level of fluorescence in Aβ-induced SH-SY5Y cells using a reactive oxygen species kit assay and BBB permeability assay, and mRNA levels of Bax, Bcl-2, caspase-3 was measured by using RT-qPCR.  Furthermore, western blot analysis was used to measure the protein expressions of Akt, Nrf2 and HO-1 in Aβ 1-42-induced SH-SY5Y cells.Results: The effect of EGb761 was investigated on the cell apoptosis induced by Aβ 1-42 andgeneration of ROS and we found that EGb761 plays a protective role against cell injury induced by Aβ 1-42. Cell apoptosis and ROS generation in SH-SY5Y cells decreased significantly with the treatment of EGb761. Furthermore, BBB permeability reduced considerably when the cells treated with EGb761 and the expression levels of Caspase-3 and Bax decreased while that of Bcl-2 were markedly increased in the Aβ 1-42-induced SH-SY5Y cells. Also, an increased in expression levels of p-Akt, Nrf2 (nucleus) and HO-1 was observed with the treatment of EGb761 in Aβ 1-42-induced SH-SY5Y cells.Conclusion: It can be concluded from these results that EGb761 could play a protective role byinhibiting apoptosis and protect Aβ 1-42-induced cell injury in vitro model of AD via activating Akt/Nrf2signaling pathway. Our study suggested that EGb761 might be a therapeutic agent for the preventionand treatment of AD.

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e79814 ◽  
Author(s):  
Li-Ting Wang ◽  
Bo-Lin Chen ◽  
Cheng-Tien Wu ◽  
Kuo-How Huang ◽  
Chih-Kang Chiang ◽  
...  

Author(s):  
Rashid Amin ◽  
Temiz A. Artmann ◽  
Gerhard Artmann ◽  
Philip Lazarovici ◽  
Peter I. Lelkes

Author(s):  
Christoph M. Zehendner ◽  
Robin White ◽  
Jana Hedrich ◽  
Heiko J. Luhmann

2003 ◽  
pp. 419-434 ◽  
Author(s):  
Matteo Marroni ◽  
Kelly M. Kight ◽  
Mohammed Hossain ◽  
Luca Cucullo ◽  
Shailesh Y. Desai ◽  
...  

2020 ◽  
Vol 14 (5) ◽  
pp. 639-644
Author(s):  
Liming Hu ◽  
Tianyi Zhao ◽  
Jia Wang ◽  
Renguang Wang ◽  
Hongshi Bu ◽  
...  

To elucidated the inhibitory effect of beauvericin (BEA) on glioma cells and its possible molecular mechanism, in this study, the MTT assay was performed to observed the effect of BEA on cell proliferation, the flow cytometry was used to measure its protective effect on cell apoptosis, and the Western Blot assay was performed to test the expression levels of signal transduction proteins. In the results, the concentration of BEA was 0.5 μmoL/L in the drug group, indicating that it has obvious protect effect to the U251 cells. The apoptosis rates of BEA, Cis and BEA+Cis groups, compared with the U251 group, were 2.93, 3.71 and 5.0 times higher respectively. In addition, the expression levels of Cyclin D1, E, B and Bcl-2 in BEA group were 75, 69, 78 and 67% of that in the U251 group, while Bax and cleaved caspase-3 were twice as much as that in the U251 group. In conclusion, beauvericin can inhibit U251 cell apoptosis and the possible mechanism is to reduce the expression of Cyclin D1, B, E and Bcl-2, while the levels of Bax and cleaved Caspase-3 increased. Thus, BEA has a broad application prospect in the treatment of glioma.


2020 ◽  
Vol 14 (5) ◽  
pp. 616-623
Author(s):  
Yun-Feng Liu ◽  
Yong-Mei Guan ◽  
Shi-Yu Huang ◽  
Lu Wu ◽  
Wei-Feng Zhu ◽  
...  

This research sought to study the influence and potentialmechanism of paeoniflorin and albiflorin on strychnine and brucine transport in MDCK-MDR1 cells regulated by P-gp. Cytotoxicity of drugs was tested by MTT assay, and the transport studies were performed in both directions in MDCK-MDR1 cells. The influence of drugs on P-gp ATPase, and the efflux function of P-gp, the expression levels of P-gp and MDR1 mRNA were also estimated. Strychnine and brucine showed well absorption, and the main transport mechanism might be passive diffusion. Verapamil could significantly decrease the efflux rate (ER) of strychnine and brucine, while the ER of strychnine and brucine was increased significantly when co-administrated with paeoniflorin or albiflorin, indicating that paeoniflorin and albiflorin could promote the efflux of these two alkaloids. Strychnine and brucine could activate the activity of P-gp ATPase, suppress the efflux function of P-gp, but have no significant effect on the expression of P-gp. In addition, strychnine could upregulate the expression of MDR1 mRNA. Paeoniflorin and albiflorin could increase the transmembrane transport of strychnine and brucine mediated by P-gp when co-administrated with strychnine or brucine via stimulating the activity of P-gp ATPase, enhancing the efflux function of P-g, increasing the expression levels of MDR1 mRNA and P-gp.


2019 ◽  
Vol 48 (2) ◽  
pp. 780-793 ◽  
Author(s):  
Monica L. Moya ◽  
Michael Triplett ◽  
Melinda Simon ◽  
Javier Alvarado ◽  
Ross Booth ◽  
...  

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