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Updated: Feb 16, 2026
Focal Cerebral Ischemia Model by Endovascular Suture Occlusion of the Middle Cerebral Artery in the Rat
Published on: February 5, 2011
Myricetin against ischemic cerebral injury in rat middle cerebral artery occlusion model
Long Sun1, Peng Xu1, Tinggang Fu1
1Department of Neurosurgery, Lin Yi Central Hospital, Linyi, Shandong 276400, P.R. China.
Abstract:
The purpose of the present study was to examine the effects of myricetin on reducing cerebral ischemia injury in a rat model. A rat model of permanent middle cerebral artery occlusion (pMCAO) was used in the present study. Rats were randomized into the following five groups: Sham, model, low‑myricetin (1 mg/kg), medium‑myricetin (5 mg/kg) and high‑myricetin (25 mg/kg) groups. Neurological deficit scores were evaluated by an examiner blinded to the experimental groups. Brain infarct size was estimated macroscopically using 2,3,5‑triphenyltetrazolium chloride staining. The levels of inflammatory factors tumor necrosis factor (TNF)‑α, interleukin (IL)‑6 and IL‑1β, and oxidative stress index superoxide dismutase (SOD), malondiadehyde (MDA), and the glutathione/glutathione disulfide (GSH/GSSG) ratio were measured by ELISA. The degree of brain cell apoptosis was determined using a terminal deoxynucleotidyl transferase dUTP nick‑end labeling assay. Protein expression levels of total or phosphorylated p38 mitogen activated protein kinase (MAPK), nuclear factor (NF)‑κB/p65 and protein kinase B (AKT) were determined using a western blotting assay. The neurological deficit score and infarct area induced by pMCAO decreased in a dose‑dependent manner following myricetin treatment. Furthermore, myricetin reduced the expression levels of IL‑1β, IL‑6, TNF‑α, and MDA, and increased GSH/GSSG ratio and SOD activity. A significant decrease in cell apoptosis was observed in response to myricetin. In addition, myricetin significantly increased the level of phosphorylated AKT protein, and decreased the phosphorylation of p38 MAPK and the level of NF‑κB/p65. Overall, the results of the present study suggested that myricetin exhibits a therapeutic effect by reducing ischemic cerebral injury, and the protective effect of myricetin may be associated with the p38 MAPK, NF‑κB/p65 and AKT signaling pathways.
Insights
Myricetin effectively reduces brain damage from stroke in rats. This natural compound lowers inflammation, oxidative stress, and cell death by influencing key signaling pathways.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Cerebral ischemia, a stroke type, causes significant brain injury.
- Effective treatments to mitigate ischemic damage are crucial.
Purpose of the Study:
- To investigate the neuroprotective effects of myricetin in a rat model of cerebral ischemia.
- To elucidate the molecular mechanisms underlying myricetin's action.
Main Methods:
- A permanent middle cerebral artery occlusion (pMCAO) rat model was established.
- Rats were treated with varying doses of myricetin.
- Neurological deficits, infarct size, inflammatory markers, oxidative stress, apoptosis, and key protein expressions (p38 MAPK, NF-κB/p65, AKT) were assessed.
Main Results:
- Myricetin dose-dependently reduced neurological deficit scores and infarct volume.
- It decreased inflammatory factors (TNF-α, IL-6, IL-1β) and oxidative stress markers (MDA).
- Myricetin increased antioxidant activity (SOD, GSH/GSSG ratio), reduced apoptosis, and modulated p38 MAPK, NF-κB/p65, and AKT signaling.
Conclusions:
- Myricetin demonstrates significant therapeutic potential against ischemic cerebral injury.
- Its protective effects are linked to the modulation of p38 MAPK, NF-κB/p65, and AKT signaling pathways.
