Cerebrolysin improves peripheral inflammatory pain: Sex differences in two models of acute and chronic mechanical hypersensitivity.

Chronic inflammatory pain is a major health problem worldwide with high prevalence in women. Cerebrolysin is a multimodal neuropeptide preparation that crosses the blood brain barrier and displays neuroprotective properties in aging and disease. Previously, we showed that cerebrolysin reduced mechanical allodynia in a model of persistent inflammation and pain. We aim to build upon the findings of our previous study by investigating the response to acute administration of cerebrolysin in two models of peripheral inflammation and assessing sex differences. We utilized the complete Freund's adjuvant (CFA) that produces maximal oedema and mechanical allodynia within days and carrageenan that produces similar effects within hours. Cerebrolysin reversed the mechanical allodynia in both sexes in CFA-treated rats. On the other hand, in rats treated with carrageenan, cerebrolysin was only effective in reducing mechanical allodynia in female rats. In conclusion, the present study shows that cerebrolysin effects may be sex-specific depending on different mechanisms that are at play in these two models of peripheral inflammatory pain. Further investigations are required to determine the factors contributing to sex differences.

Cerebrolysin reduces mechanical allodynia in a rodent model of peripheral inflammation.

Cerebrolysin (Cbl) is a neuropeptide preparation of cerebroproteins that crosses the blood brain barrier displaying neuroprotective properties and promoting neurogenesis. Limited evidence exists on the efficacy of Cbl for the treatment of pain, with many studies focusing on neuropathic pain associated to diabetes. Therefore, we designed a study to test the hypothesis that Cbl would reduce mechanical allodynia in a rat model of peripheral inflammation induced by administration of complete Freund's adjuvant (CFA) in the hind paw. We found that acute administration of Cbl was effective in reducing mechanical allodynia but not peripheral inflammation in the CFA model of inflammatory pain. Our investigation supports further investigation into the therapeutic applications and mechanisms underlying the anti-allodynic effects of Cbl in inflammatory pain.