Heparin-Modified Superparamagnetic Iron Oxide Nanoparticles Suppress Lithium Chloride/Pilocarpine-Induced Temporal Lobe Epilepsy in Rats through Attenuation of Inflammation and Oxidative Stress.
Hanbing XuYubo WangCongcong YuChunhong HanHuifei CuiPublished in: ACS chemical neuroscience (2024)
The development of antiepileptic drugs is still a long process. In this study, heparin-modified superparamagnetic iron oxide nanoparticles (UFH-SPIONs) were prepared, and their antiepileptic effect and underlying mechanism were investigated. UFH-SPIONs are stable, homogeneous nanosystems with antioxidant enzyme activity that are able to cross the blood-brain barrier (BBB) and enriched in hippocampal epileptogenic foci. The pretreatment with UFH-SPIONs effectively prolonged the onset of seizures and reduced seizure severity after lithium/pilocarpine (LP)-induced seizures in rats. The pretreatment with UFH-SPIONs significantly decreased the expression of inflammatory factors in hippocampal tissues, including IL-6, IL-1β, and TNF-α. LP-induced oxidative stress in hippocampal tissues was in turn reduced upon pretreatment with UFH-SPIONs, as evidenced by an increase in the levels of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) and a decrease in the level of lipid peroxidation (MDA). Moreover, the LP-induced upregulation of apoptotic cells was decreased upon pretreatment with UFH-SPIONs. Together, these observations suggest that the pretreatment with UFH-SPIONs ameliorates LP-induced seizures and downregulates the inflammatory response and oxidative stress, which exerts neuronal protection during epilepsy.
Keyphrases
- oxidative stress
- temporal lobe epilepsy
- diabetic rats
- iron oxide nanoparticles
- high glucose
- induced apoptosis
- inflammatory response
- gene expression
- dna damage
- ischemia reperfusion injury
- drug induced
- poor prognosis
- venous thromboembolism
- signaling pathway
- hydrogen peroxide
- rheumatoid arthritis
- endothelial cells
- anti inflammatory
- growth factor
- high resolution
- mouse model
- toll like receptor
- lipopolysaccharide induced
- cell cycle arrest
- subarachnoid hemorrhage
- cerebral ischemia
- stress induced
- lps induced
- living cells
- heat shock
- binding protein