Chunzhen Zhao
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Chunzhen Zhao has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
Lin Wang
Weifang Medical University
2 shared publicationsHai-Jian Li
1 shared publication- Haijian Li
National Key Laboratory of Energetic Materials, Xi’an Modern Chemistry Research Institute, Xi’an 710065, China
1 shared publication Jincheng Jincheng
Department of Pharmacology and Laboratory of Applied Pharmacology
1 shared publicationJingjing Ming
Weifang Medical University
1 shared publicationJingjing Su
Key Laboratory of Molecular Pharmacology and Translational Medicine and Department of Pharmacology, College of Pharmacy, Shandong Second Medical University, Weifang , 261053, China
1 shared publication
Latest Publications
- Open Access
- 12 June 2024
- Published by Elsevier in Stem Cell Research
- Vol. 79, 103469
Systemic knockout of Tmem175 results in aberrant differentiation but no effect on hematopoietic reconstitution
- 12 June 2024
- Published by Elsevier in Stem Cell Research
- Vol. 79, 103469
Open AccessSystemic knockout of Tmem175 results in aberrant differentiation but no effect on hematopoietic reconstitution
- 13 October 2022
- Published by Springer Nature
- p. 1147-1154
Online Intelligent Classroom Teaching Innovation of Pharmacy Based on Artificial Intelligence Technology
- 13 October 2022
- Published by Springer Nature
- p. 1147-1154
Online Intelligent Classroom Teaching Innovation of Pharmacy Based on Artificial Intelligence Technology
- Open Access
- 31 March 2021
- Published by Creative Publishing Co., Limited in Medical Research
- Vol. 3 (1) , 1-5
The Temporal Profile of OPG Expression and Regulatory Role on Ischemic Brain Injury in Rats After MCAo
- 31 March 2021
- Published by Creative Publishing Co., Limited in Medical Research
- Vol. 3 (1) , 1-5
Open AccessThe Temporal Profile of OPG Expression and Regulatory Role on Ischemic Brain Injury in Rats After MCAo
- 31 December 2019
- Published by Creative Publishing Co., Limited in Medical Research
- Vol. 1 (1) , 12-17
1,8-Cineol Attenuated AΒ25-35-Induced PC12 Cell Injury through Reducing Caspase 3 Expression and NO Production
Objective To investigate the effect of 1,8-cineol on caspase 3 expression and NO production induced by Aβ25-35 in PC12 cells. Methods PC12 cells were cultured in vitro, and cell injury was induced by Aβ25-35 with a concentration of 20 μM. 1,8-cineol (1, 3, 10 μM) was pretreated before Aβ25-35 treatment. PC12 cell viability was evaluated by MTT detection assay. Caspase 3 protein expression was detected by Western blotting. The level of NO production in PC12 cells was measured using ELISA detection assay kit. Results In cultured PC12 cells in vitro, MTT results showed that 20 μM of Aβ25-35 reduced cell viability significantly compared with control group. The cell viability was increased by pretreatment with 1,8-cineol with concentrations of 3 and 10 μM compared with Aβ25-35 only group. Western blotting results showed compared with control group, caspase 3 expression was increased significantly in 20 μM Aβ25-35 group. Compared with Aβ25-35 group, 1,8-cineol of 3 and 10 μM group reduced caspase 3 protein expression significantly. The level of NO production in PC12 cells was increased significantly, which was decreased by pretreatment with 3 and 10 μM of 1,8-cineol. Conclusions: Our results revealed a protective effect of 1,8-cineol on Aβ25-35 induced PC12 cell injury through inhibition of caspase 3 expression and NO production.
- 31 December 2019
- Published by Creative Publishing Co., Limited in Medical Research
- Vol. 1 (1) , 12-17
1,8-Cineol Attenuated AΒ25-35-Induced PC12 Cell Injury through Reducing Caspase 3 Expression and NO Production
Objective To investigate the effect of 1,8-cineol on caspase 3 expression and NO production induced by Aβ25-35 in PC12 cells. Methods PC12 cells were cultured in vitro, and cell injury was induced by Aβ25-35 with a concentration of 20 μM. 1,8-cineol (1, 3, 10 μM) was pretreated before Aβ25-35 treatment. PC12 cell viability was evaluated by MTT detection assay. Caspase 3 protein expression was detected by Western blotting. The level of NO production in PC12 cells was measured using ELISA detection assay kit. Results In cultured PC12 cells in vitro, MTT results showed that 20 μM of Aβ25-35 reduced cell viability significantly compared with control group. The cell viability was increased by pretreatment with 1,8-cineol with concentrations of 3 and 10 μM compared with Aβ25-35 only group. Western blotting results showed compared with control group, caspase 3 expression was increased significantly in 20 μM Aβ25-35 group. Compared with Aβ25-35 group, 1,8-cineol of 3 and 10 μM group reduced caspase 3 protein expression significantly. The level of NO production in PC12 cells was increased significantly, which was decreased by pretreatment with 3 and 10 μM of 1,8-cineol. Conclusions: Our results revealed a protective effect of 1,8-cineol on Aβ25-35 induced PC12 cell injury through inhibition of caspase 3 expression and NO production.