The total flavones of Abelmoschus manihot inhibit reactive proliferation of astrocytes following cerebral ischemia

Weizhuo Lu; Jingru Tong; Miaomiao Zhou; Jiyue Wen

Articles

Abstract

Pharmacognosy Magazine,2022,18,79,752-757.

DOI:10.4103/pm.pm_572_21

Published:September 2022

Type:Original Article

Authors:

Author(s) affiliations:

Weizhuo Lu¹, Jingru Tong², Miaomiao Zhou³, Jiyue Wen⁴
¹Medical Branch, Hefei Technology College, Hefei, China
²Department of Bioengineering, College of Life Science, Huaibei Normal University, Huaibei, China
³Department of Nursing, West Anhui Health Vocational College, Liuan, China
⁴Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, China

Abstract:

Objective: The aim of this study was to demonstrate the role of the total flavones of Abelmoschus manihot (TFA) in the reactive proliferation of astrocytes after cerebral ischemia in mice. Materials and Methods: The expression of glial fibrillary acidic protein (GFAP) and secretion of chondroitin sulfate proteoglycans (CSPGs) from astrocytes in brain tissues were used to evaluate the effect of TFA on the reactive proliferation of astrocytes after cerebral ischemia. Besides, we detected the activities of angiotensin-converting enzyme (ACE) and ACE2 and production of angiotensin (Ang)-II and Ang-(1–7) in the brain tissues. Furthermore, the role of Ang-(1–7) and TFA in GFAP expression and proliferation of primary cultured astrocytes under hypoxia induced by cobalt chloride (CoCl₂) was tested. Results: Cerebral ischemia induced a significant increase of GFAP expression and CSPGs secretion in mice brain tissues, which was inhibited by TFA treatment. In addition, TFA treatment inhibited the increment of ACE activity and Ang II production induced by ischemia in the brain tissues; likewise, TFA induced a significant upregulation of ACE2 activity and Ang-(1–7) production. Furthermore, TFA or Ang-(1–7) treatment markedly reduced reactive proliferation of astrocytes under hypoxia. Conclusion: TFA inhibits reactive proliferation of astrocytes in the brain tissues following cerebral ischemia by upregulating ACE2/Ang-(1–7).