Table 2.
Pathways involved in stroke and possible roles of DHA. Relevant references are provided in the text.
| Pathway | Effect of DHA |
|---|---|
| Production of arachidonic acid (AA) | ↓ |
| • AA liberation from membrane phospholipids | ↓ |
| • Free AA levels | ↓ |
| • Pro-inflammatory eicosanoids | ↓ |
| Ionic homeostasis | ↑ |
| • Na+-K+ ATPase activity | ↑ |
| • Ionic imbalance (Na+, K+) | ↓ |
| • Increased intracellular Ca2+ | ↓ |
| • Cell edema | ↓ |
| Glutamate receptor and synaptic activity | ↓ |
| • Glutamate release | ↓ |
| • Impaired glutamate reuptake at presynaptic nerve endings | ↓ |
| • Glutamate receptors stimulation | ↓ |
| • Influx of Ca2+ into cells | ↓ |
| Apoptosis | ↓ |
| • Pro-apoptotic Bcl-2 gene induction | ↓ |
| • Anti-apoptotic Bcl-2 gene induction | ↑ |
| • Expression of anti-apoptotic Bcl-2 protein | ↑ |
| Mitochondrial function | ↑ |
| • Intracellular Ca2+ balance | ↑ |
| • Cytochrome c release | ↓ |
| • Pro-apoptotic caspases | ↓ |
| Formation of free radicals | ↓ |
| • ROS production | ↓ |
| • Anti-oxidant molecules | ↑ |
| Inflammatory mediators | ↓ |
| • Leukocyte infiltration | ↓ |
| • IL-1β expression | ↓ |
| • COX-2-induced prostaglandins | ↓ |
| • NF-kB activity | ↓ |
| • Microglial activation | ↓ |
| Cerebral infarction volume | ↓ |