Investigation of the protective effects of piceatannol on experimental subarachnoid hemorrhage in rats

Erbil G., UZUN M.

Molecular Biology Reports, vol.51, no.1, 2024 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 51 Issue: 1
  • Publication Date: 2024
  • Doi Number: 10.1007/s11033-024-09275-1
  • Journal Name: Molecular Biology Reports
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, Veterinary Science Database
  • Keywords: Apoptosis, Edema, Hippocampus, Inflammation, Piceatannol, Pyknosis, Subarachnoid hemorrhage
  • Çanakkale Onsekiz Mart University Affiliated: Yes


Background: Subarachnoid hemorrhage (SAH) is one of the most prevalent brain injuries in humans which has poor prognosis and high mortality rates. Due to several medical or surgical treatment methods, a gold standard method doesn’t exist for SAH treatment. Piceatannol (PCN), a natural analog of resveratrol, was reported to reduce inflammation and apoptosis promising a wide range of therapeutic alternatives. In this study, we aimed to investigate the effects of PCN in an experimental SAH model. The alleviating effects of PCN in the hippocampus in an experimental SAH model were investigated for the first time. Methods and results: In this study, 27 Wistar Albino male rats (200–300 g; 7–8 week) were used. Animals were divided into three groups; SHAM, SAH, and SAH + PCN. SAH model was created with 120 µl of autologous arterial tail blood to prechiasmatic cisterna. 30 mg/kg PCN was administered intraperitoneally at 1st h after SAH. Neurological evaluation was performed with Garcia's score. RT-PCR was performed for gene expression levels in the hippocampus. Pyknosis, edema, and apoptosis were evaluated by H&E and TUNEL staining. Our results indicated that PCN administration reduced apoptosis (P < 0.01), cellular edema, and pyknosis (P < 0.05) in the hippocampus after SAH. Moreover, PCN treatment significantly decreased the expression levels of TNF-α (P < 0.01), IL-6 (P < 0.05), NF-κB (P < 0.05), and Bax (P < 0.05) in the hippocampus. Conclusions: Our results demonstrated that PCN might be a potential therapeutic adjuvant agent for the treatment of early brain injury (EBI) following SAH. Further studies are required to clarify the underlying mechanisms and treatment options of SAH.