Home | About PM | Editorial board | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Advertise | Contact us |  Login 
Pharmacognosy Magazine
Search Article 
Advanced search 
Year : 2022  |  Volume : 18  |  Issue : 79  |  Page : 752-757

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

1 Medical Branch, Hefei Technology College, Hefei, China
2 Department of Bioengineering, College of Life Science, Huaibei Normal University, Huaibei, China
3 Department of Nursing, West Anhui Health Vocational College, Liuan, China
4 Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, China

Correspondence Address:
Jiyue Wen
Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_572_21

Rights and Permissions

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).

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded11    
    Comments [Add]    

Recommend this journal