Novel synthetic analogue of ACTH 4-10 (Semax) but not glycine prevents the enhanced nitric oxide generation in cerebral cortex of rats with incomplete global ischemia.
Bashkatova. V G VG; Koshelev. V B VB; Fadyukova. O E OE; Alexeev. A A AA; Vanin. A F AF; Rayevsky. K S KS; Ashmarin. I P IP; Armstrong. D M DM
Key Findings
- Global ischemia in rats raises nitric oxide levels and lipid peroxidation markers.
- Glycine does not reduce nitric oxide or improve neurological outcomes after ischemia.
- Semax significantly reduces nitric oxide rise and restores neurological function in the same model.
Practical Outcomes
- Semax shows promise as a neuroprotective agent in animal models of brain ischemia, hinting it could help protect the brain after events like strokes. However, human studies are needed, and no dosing guidelines exist for healthy people, so it’s not ready for everyday use yet.
Summary
In rats that suffered a brief loss of blood flow to the brain, the drug Semax lowered the surge of nitric oxide (a molecule that can damage cells) and helped the animals recover better, while a simple amino acid, glycine, did nothing. This suggests Semax might protect brain cells after a stroke‑like event by controlling harmful chemicals.
Abstract
This work investigates whether nitric oxide production and lipid peroxidation contribute to the pathophysiology of ischemia and whether glycine and a novel Russian compound, Semax are neuroprotective via a mechanism involving the regulation nitric oxide (NO) and lipid peroxidation. In brief, nitric oxide and indices of lipid peroxidation were elevated following global ischemia. While glycine proved ineffective in reducing NO levels or ameliorating the neurological deficits following global ischemia, Semax proved to be highly effective in abating the rise in nitric oxide and restoring neurologic functioning.
Study Information
pubmed
2001
2001-03-09T00:00:00.000Z
10.1016/s0006-8993(00)03324-2