Hydrogen sulfide attenuates induction and prevents progress of the 6-hydroxydopamine-induced Parkinsonism in rat through activation of ATP-sensitive potassium channels and suppression of ER stress

Studies argue in favor of hydrogen sulfide (H2S) as the next potent therapeutic agent for neurodegenerative diseases. In present study, we investigated effect long term treatment with NaHS (as donor H2S) on induction and progress 6-hydroxydopamine (6-OHDA) -induced Parkinsonism rat. The 6-OHDA was injected into medial forebrain bundle right hemisphere by stereotaxic surgery. Behavioral tests treatments were carried out to eight weeks after toxin. Immunohistochemistry western blotting evaluate survival tyrosine hydroxylase (TH) -positive neurons substantia nigra (SN) also expression glucose-regulated protein 78 (GRP78) C/EBP homologous (CHOP), markers endoplasmic reticulum (ER) stress, striatum SN. Eight assessment behavioral symptoms showed that especially at dose 100 ?mol/kg attenuates remarkably prevents its progress. increased TH- positive suppressed 6-OHDA- induced overexpression GRP78 CHOP. Blockade ATP-sensitive potassium (K-ATP) channels glibenclamide (Glib) prevented markedly both phase neurons. But Glib did not affect preventing suppressing ER stress markers. H2S increases dopaminergic through activation K-ATP channels. probably suppression stress.