[Semax prevents elevation of nitric oxide generation caused by incomplete global ischemia in the rat brain].
Fadiukova. O E OE; Alekseev. A A AA; Bashkatova. V G VG; Tolordava. I A IA; Kuzenkov. V S VS; Mikoian. V D VD; Vanin. A F AF; Koshelev. V B VB; Raevskiĭ. K S KS
Key Findings
- Incomplete global brain ischemia in rats caused a two‑fold rise in nitric oxide and a moderate increase in lipid‑peroxidation products.
- Higher brain NO levels were linked to worse neurological symptoms in the ischemic rats.
- A single dose of semax (0.3 mg/kg) blocked both the excess NO production and the development of neurological disturbances.
Practical Outcomes
- The study suggests semax may have neuroprotective properties by limiting NO‑driven damage after a brief loss of blood flow to the brain. However, the work is limited to rats and uses a specific ischemia model, so it does not directly translate into a ready‑to‑use protocol for humans. Biohackers should view this as early‑stage evidence that warrants further clinical research before considering dosage or supplementation.
Summary
In rats that had reduced blood flow to the brain, a spike in nitric oxide (NO) and some damage‑related chemicals showed up, and the animals displayed neurological problems. Giving them the synthetic peptide semax (0.3 mg per kg) stopped the NO surge and prevented the brain‑related symptoms.
Abstract
A twofold increase in the nitric oxide (NO) production and a moderate increase in the content of secondary products of lipid peroxidation was observed in Wistar rats with incomplete global ischemia model induced by the bilateral occlusion of common carotid arteries. A clear correlation was observed between the NO content in the rat brain and the level of neurological disturbance manifestations in the ischemized animals. The synthetic peptide semax (a fragment of ACTH4-7 Pro-Gly-Pro) in a dose of 0.3 mg/kg prevented from the development of both neurological disturbances and excess NO production in the rat brain cortex.
Study Information
pubmed
2001