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Background: Ischemic stroke presents a significant threat to human health due to its high disability rate and mortality. Currently, the clinical treatment drug, rt-PA, has a narrow therapeutic window and carries a high risk of bleeding. There is an urgent need to find new effective therapeutic drugs for ischemic stroke. Icariin (ICA), a key ingredient in the traditional Chinese medicine Epimedium, undergoes metabolism in vivo to produce Icaritin (ICT). While ICA has been reported to inhibit neuronal apoptosis after cerebral ischemia-reperfusion (I/R), yet its underlying mechanism remains unclear.

Methods: PC-12 cells were treated with 200 µM H 2 O 2 for 8 h to establish a vitro model of oxidative damage. After administration of ICT, cell viability was detected by Thiazolyl blue tetrazolium Bromide (MTT) assay, reactive oxygen species (ROS) and apoptosis level, mPTP status and mitochondrial membrane potential (MMP) were detected by flow cytometry and immunofluorescence. Apoptosis and mitochondrial permeability transition pore (mPTP) related proteins were assessed by Western blotting. Middle cerebral artery occlusion (MCAO) model was used to establish I/R injury in vivo. After the treatment of ICA, the neurological function was scored by ZeaLonga socres; the infarct volume was observed by 2,3,5-Triphenyltetrazolium chloride (TTC) staining; HE and Nissl staining were used to detect the pathological state of the ischemic cortex; the expression changes of mPTP and apoptosis related proteins were detected by Western blotting.

Results: In vitro: ICT effectively improved H 2 O 2 -induced oxidative injury through decreasing the ROS level, inhibiting mPTP opening and apoptosis. In addition, the protective effects of ICT were not enhanced when it was co-treated with mPTP inhibitor Cyclosporin A (CsA), but reversed when combined with mPTP activator Lonidamine (LND). In vivo: Rats after MCAO shown cortical infarct volume of 32-40%, severe neurological impairment, while mPTP opening and apoptosis were obviously increased. Those damage caused was improved by the administration of ICA and CsA.

Conclusions: ICA improves cerebral ischemia-reperfusion injury by inhibiting mPTP opening, making it a potential candidate drug for the treatment of ischemic stroke.

Titel:	Icariin improves oxidative stress injury during ischemic stroke via inhibiting mPTP opening.
Autor/in / Beteiligte Person:	Zhou, Z ; Li, W ; Ni, L ; Wang, T ; Huang, Y ; Yu, Y ; Hu, M ; Liu, Y ; Wang, J ; Huang, X ; Wang, Y
Link:	Zum Volltext
Zeitschrift:	Molecular medicine (Cambridge, Mass.), Jg. 30 (2024-06-05), Heft 1, S. 77
Veröffentlichung:	2018- : [London, United Kingdom] : BioMed Central ; <i>Original Publication</i>: Cambridge, Mass. : Blackwell Scientific Publications, c1994-, 2024
Medientyp:	academicJournal
ISSN:	1528-3658 (electronic)
DOI:	10.1186/s10020-024-00847-2
Schlagwort:	Animals Rats PC12 Cells Male Reperfusion Injury metabolism Reperfusion Injury drug therapy Disease Models, Animal Hydrogen Peroxide metabolism Cell Survival drug effects Mitochondrial Membrane Transport Proteins metabolism Neuroprotective Agents pharmacology Neuroprotective Agents therapeutic use Rats, Sprague-Dawley Oxidative Stress drug effects Flavonoids pharmacology Flavonoids therapeutic use Mitochondrial Permeability Transition Pore metabolism Apoptosis drug effects Ischemic Stroke drug therapy Ischemic Stroke metabolism Ischemic Stroke etiology Reactive Oxygen Species metabolism Membrane Potential, Mitochondrial drug effects
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [Mol Med] 2024 Jun 05; Vol. 30 (1), pp. 77. <i>Date of Electronic Publication: </i>2024 Jun 05. MeSH Terms: Oxidative Stress* / drug effects ; Flavonoids* / pharmacology ; Flavonoids* / therapeutic use ; Mitochondrial Permeability Transition Pore* / metabolism ; Apoptosis* / drug effects ; Ischemic Stroke* / drug therapy ; Ischemic Stroke* / metabolism ; Ischemic Stroke* / etiology ; Reactive Oxygen Species* / metabolism ; Membrane Potential, Mitochondrial* / drug effects ; Animals ; Rats ; PC12 Cells ; Male ; Reperfusion Injury / metabolism ; Reperfusion Injury / drug therapy ; Disease Models, Animal ; Hydrogen Peroxide / metabolism ; Cell Survival / drug effects ; Mitochondrial Membrane Transport Proteins / metabolism ; Neuroprotective Agents / pharmacology ; Neuroprotective Agents / therapeutic use ; Rats, Sprague-Dawley References: Neuropharmacology. 2010 Jul-Aug;59(1-2):70-6. 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(PMID: 20354546) Grant Information: A23-1-075 the Yichang Medical and Health Research Project; SXZ202307 Open Fund of Hubei Clinical Research Center for Functional Digestive Diseases of Traditional Chinese Medicine & Hospital of Traditional Chinese Medicine of Three Gorges University Contributed Indexing: Keywords: Cerebral ischemia-reperfusion; Icariin; Ischemic stroke; Mitochondrial permeability transition pore; ROS Substance Nomenclature: VNM47R2QSQ (icariin) ; 0 (Flavonoids) ; 0 (Mitochondrial Permeability Transition Pore) ; 0 (Reactive Oxygen Species) ; BBX060AN9V (Hydrogen Peroxide) ; 0 (Mitochondrial Membrane Transport Proteins) ; 0 (Neuroprotective Agents) Entry Date(s): Date Created: 20240605 Date Completed: 20240606 Latest Revision: 20240608 Update Code: 20240608 PubMed Central ID: PMC11155182

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Icariin improves oxidative stress injury during ischemic stroke via inhibiting mPTP opening.