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Nano-Formulated Apelin13 Reduces Cerebral Ischemia/Reperfusion Injury in Rats by Suppressing Activity of
Elham Kashafi Jahromi1, Solmaz Nasseri Maleki2,3, Michael R Hamblin4
1Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Introduction:
Nanocarrier-mediated delivery represents a promising strategy for enhancing the therapeutic efficacy of pharmacological agents. This study investigated whether encapsulating the endogenous peptide apelin-13 in niosomes (Nano-Apelin13) could improve its protective effects against ischemic stroke injury in rats.
Methods:
Transient focal cerebral ischemia was induced by 60-minute middle cerebral artery occlusion (MCAO) followed by 24-hour reperfusion. Sixty rats were randomly allocated into five experimental groups: Sham, CI/R (ischemia/reperfusion), CI/R + empty niosomes, CI/R + free Apelin13, and CI/R + Nano-Apelin13. Free Apelin13 and Nano-Apelin13 (40 µg/kg) were administered intravenously 1 hour after reperfusion onset. After 24 hours, cerebral infarction size, neurological deficit scores, brain water content, and neuronal damage were evaluated. Protein expression levels of TLR4, MyD88, NF-κB, TNF-α, and IL-1β were analyzed by western blotting.
Results:
Both free Apelin13 and Nano-Apelin13 significantly reduced cerebral infarct volume, improved neurological scores, decreased neuronal loss, and downregulated MyD88 and NF-κB expression. However, Nano-Apelin13 demonstrated superior efficacy, normalizing several parameters to sham-operated levels. Notably, Nano-Apelin13 significantly suppressed TLR4 expression and attenuated cerebral edema and pro-inflammatory cytokine production, effects that were either significantly enhanced or absent in the free Apelin13-treated group.
Conclusion:
Delivery of Apelin13 in niosomes could be a good option to reduce CI/R damage by inhibiting the activity of TLR4/MyD88/NF-kB axis compared to free Apelin13.