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Original Research Article | OPEN ACCESS

Proteasome activator 28A: A clinical biomarker and pharmaceutical target in acute cerebral infarction therapy

Cuiping Guo1 , Jianghong Han1, Jie Xu2, Zhiyao Yuan1, Dan Li1, Qiang Liu3, Zhenghui Wang4

1Sanquan College of Xinxiang Medical University, Xinxiang, China; 2Department of Ultrasound Medicine, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China; 3Department of Rehabilitation, Henan No. 3 Provincial People's Hospital, Zhengzhou, China; 4Department of Rehabilitation, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.

For correspondence:-  Cuiping Guo   Email: 1063115309@qq.com   Tel:+8613781959825

Accepted: 25 September 2022        Published: 28 October 2022

Citation: Guo C, Han J, Xu J, Yuan Z, Li D, Liu Q, et al. Proteasome activator 28A: A clinical biomarker and pharmaceutical target in acute cerebral infarction therapy. Trop J Pharm Res 2022; 21(10):2219-2225 doi: 10.4314/tjpr.v21i10.24

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To determine the dynamic changes in serum levels of PA28α in patients with acute cerebral infarction (ACI), and to investigate its correlation with infarct size and neurological deficit of the disease.
Methods: A total of 100 ACI patients and 100 healthy volunteers were recruited from The First Affiliated Hospital of Xinxiang Medical University as case and control groups, respectively. Their serum levels of PA28α were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The potential of PA28α in predicting the incidence of ACI was assessed by plotting ROC curves. Multivariate logistic regression analysis was conducted to investigate the risk factors of ACI. In addition, an ACI model in rats was established, and ACI rats were classified into 1, 3, 5, 7 and 14 day subgroups based on the duration post-ACI. Rats in the sham group served as control.
Results: Serum level of PA28α was significantly higher in ACI patients than in controls. Moreover, the serum level of PA28α at admission was positively correlated to the NIHSS score and infarct volume of ACI patients. The level of PA28α in ACI rats gradually increased post-ACI, reaching a peak on day 7. The number of apoptotic brain cells in ACI rats gradually decreased after ACI. In addition, PA28α level was negatively correlated to the number of apoptotic brain cells in ACI rats (R2 = 0.5148, p < 0.001).  
Conclusion: The serum level of PA28α is elevated in ACI patients, and is positively correlated to infarct volume and neurological deficit of the disease. The dynamic change in brain cell apoptosis post-ACI is negatively correlated to the serum level of PA28α. These findings may provide theoretical basis for the diagnosis and treatment of ACI.

Keywords: Acute cerebral infarction, Proteasome activator 28A, Biomarker, Pharmaceutical target, Apoptotic brain cells

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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