Simvastatin-loaded nano-niosomes efficiently downregulates the MAPK-NF-κB pathway during the acute phase of myocardial ischemia-reperfusion injury.


Journal

Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234

Informations de publication

Date de publication:
Nov 2022
Historique:
received: 23 04 2022
accepted: 18 08 2022
revised: 10 08 2022
pubmed: 13 9 2022
medline: 2 11 2022
entrez: 12 9 2022
Statut: ppublish

Résumé

Simvastatin can potentially mitigate acute inflammatory phase of myocardial ischemia-reperfusion injury. However, these effects negatively influenced by its poor bioavailability, low water solubility and high metabolism. Here, we investigated the effects of SIM-loaded nano-niosomes on a rat model of MI/R injury to find a drug delivery method to tackle the barriers. Nano-niosomes' characteristics were identified using dynamic light scattering and transmission electron microscopy. Fifty male Wistar rats were divided into five groups: Sham; MI/R; MI/R + nano-niosome; MI/R + SIM; MI/R + SIM-loaded nano-niosomes. Left anterior descending artery was ligated for 45 min, and 3 mg/kg SIM, nano-niosomes, or SIM-loaded nano-niosomes was intramyocardially injected ten min before the onset of reperfusion. ELISA assay was used to assess cardiac injury markers (cTnI, CK-MB) and inflammatory cytokines (TNF-α, IL-6, TGF-β, MPC-1). Expression level of MAPK-NF-κB and histopathological changes were evaluated by western blot and hematoxylin & eosin staining, respectively. the size of nano-niosome was 137 nm, reached to 163 nm when simvastatin was loaded. To achieve optimized niosomes span 80, a drug/cholesterol ratio of 0.4 and seven min of sonication time was applied. Optimized entrapment efficiency of SIM-loaded nano-niosomes was 98.21%. Inflammatory cytokines and the expression level of MAPK and NF-κB were reduced in rats receiving SIM-loaded nano-niosomes compared to MI/R + SIM and MI/R + SIM-loaded nano-niosomes. Our results showed that SIM-loaded nano-niosomes could act more efficiently than SIM in alleviating the acute inflammatory response of reperfusion injury via downregulating the activation of MAPK-NF-κB.

Sections du résumé

BACKGROUND BACKGROUND
Simvastatin can potentially mitigate acute inflammatory phase of myocardial ischemia-reperfusion injury. However, these effects negatively influenced by its poor bioavailability, low water solubility and high metabolism. Here, we investigated the effects of SIM-loaded nano-niosomes on a rat model of MI/R injury to find a drug delivery method to tackle the barriers.
METHODS METHODS
Nano-niosomes' characteristics were identified using dynamic light scattering and transmission electron microscopy. Fifty male Wistar rats were divided into five groups: Sham; MI/R; MI/R + nano-niosome; MI/R + SIM; MI/R + SIM-loaded nano-niosomes. Left anterior descending artery was ligated for 45 min, and 3 mg/kg SIM, nano-niosomes, or SIM-loaded nano-niosomes was intramyocardially injected ten min before the onset of reperfusion. ELISA assay was used to assess cardiac injury markers (cTnI, CK-MB) and inflammatory cytokines (TNF-α, IL-6, TGF-β, MPC-1). Expression level of MAPK-NF-κB and histopathological changes were evaluated by western blot and hematoxylin & eosin staining, respectively.
RESULTS RESULTS
the size of nano-niosome was 137 nm, reached to 163 nm when simvastatin was loaded. To achieve optimized niosomes span 80, a drug/cholesterol ratio of 0.4 and seven min of sonication time was applied. Optimized entrapment efficiency of SIM-loaded nano-niosomes was 98.21%. Inflammatory cytokines and the expression level of MAPK and NF-κB were reduced in rats receiving SIM-loaded nano-niosomes compared to MI/R + SIM and MI/R + SIM-loaded nano-niosomes.
CONCLUSION CONCLUSIONS
Our results showed that SIM-loaded nano-niosomes could act more efficiently than SIM in alleviating the acute inflammatory response of reperfusion injury via downregulating the activation of MAPK-NF-κB.

Identifiants

pubmed: 36097124
doi: 10.1007/s11033-022-07891-3
pii: 10.1007/s11033-022-07891-3
doi:

Substances chimiques

NF-kappa B 0
Simvastatin AGG2FN16EV
Liposomes 0
Cytokines 0

Types de publication

Journal Article Retracted Publication

Langues

eng

Sous-ensembles de citation

IM

Pagination

10377-10385

Commentaires et corrections

Type : RetractionIn

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Nature B.V.

Références

Safiri S et al (2022) Burden of ischemic heart disease and its attributable risk factors in 204 countries and territories, 1990–2019. Eur J Prev Cardiol 29(2):420–431
pubmed: 34922374 doi: 10.1093/eurjpc/zwab213
He J et al (2022) Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review). Exp Ther Med 23(6):430
pubmed: 35607376 pmcid: 9121204 doi: 10.3892/etm.2022.11357
Lodrini AM, Goumans MJ (2021) Cardiomyocytes Cellular Phenotypes After Myocardial Infarction. Front Cardiovasc Med 8:750510
pubmed: 34820429 pmcid: 8606669 doi: 10.3389/fcvm.2021.750510
Hausenloy DJ, Yellon DM (2013) Myocardial ischemia-reperfusion injury: a neglected therapeutic target. J Clin Investig 123(1):92–100
pubmed: 23281415 pmcid: 3533275 doi: 10.1172/JCI62874
Adameova A et al (2022) Interplay of Oxidative Stress and Necrosis-like Cell Death in Cardiac Ischemia/Reperfusion Injury: A Focus on Necroptosis.Biomedicines, 10(1)
Soares RO et al (2019) Ischemia/reperfusion injury revisited: an overview of the latest pharmacological strategies. Int J Mol Sci 20(20):5034
pubmed: 31614478 pmcid: 6834141 doi: 10.3390/ijms20205034
Duan J-S et al (2019) Urotensin-# receptor antagonist SB-706375 protected isolated rat heart from ischaemia–reperfusion injury by attenuating myocardial necrosis via RhoA/ROCK/RIP3 signalling pathway. Inflammopharmacology 27(6):1309–1318
pubmed: 31168686 doi: 10.1007/s10787-019-00598-1
Su X et al (2022) Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury and Application of Natural Plant Products. Oxid Med Cell Longev, 2022: p. 8726564
Mata A, Cadenas S (2021) The Antioxidant Transcription Factor Nrf2 in Cardiac Ischemia-Reperfusion Injury.Int J Mol Sci, 22(21)
Nazarinia D et al (2021) FoxO1 and Wnt/β-catenin signaling pathway: molecular targets of human amniotic mesenchymal stem cells-derived conditioned medium (hAMSC-CM) in protection against cerebral ischemia/reperfusion injury. J Chem Neuroanat 112:101918
pubmed: 33421540 doi: 10.1016/j.jchemneu.2021.101918
Dong LY et al (2013) Cardioprotection of vitexin on myocardial ischemia/reperfusion injury in rat via regulating inflammatory cytokines and MAPK pathway. Am J Chin Med 41(6):1251–1266
pubmed: 24228599 doi: 10.1142/S0192415X13500845
Ma L et al (2014) Ginsenoside Rb3 protects cardiomyocytes against ischemia-reperfusion injury via the inhibition of JNK-mediated NF-kappaB pathway: a mouse cardiomyocyte model. PLoS ONE 9(8):e103628
pubmed: 25084093 pmcid: 4118887 doi: 10.1371/journal.pone.0103628
Ramli FF, Ali A, Ibrahim N (2022) Molecular-Signaling Pathways of Ginsenosides Rb in Myocardial Ischemia-Reperfusion Injury: A Mini Review. Int J Med Sci 19(1):65–73
pubmed: 34975299 pmcid: 8692112 doi: 10.7150/ijms.64984
Chen Z et al (2022) Inhibition of Myocardial Cell Apoptosis Is Important Mechanism for Ginsenoside in the Limitation of Myocardial Ischemia/Reperfusion Injury. Front Pharmacol 13:806216
pubmed: 35300297 pmcid: 8921549 doi: 10.3389/fphar.2022.806216
Sadrkhanloo M et al (2022) Targeting Nrf2 in ischemia-reperfusion alleviation: From signaling networks to therapeutic targeting. Life Sci 300:120561
pubmed: 35460707 doi: 10.1016/j.lfs.2022.120561
Khan SI et al (2017) Febuxostat Modulates MAPK/NF-kappaBp65/TNF-alpha Signaling in Cardiac Ischemia-Reperfusion Injury. Oxid Med Cell Longev 2017:8095825
pubmed: 29138678 pmcid: 5613710 doi: 10.1155/2017/8095825
Cai Z et al (2014) Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis. Nat Cell Biol 16(1):55–65
pubmed: 24316671 doi: 10.1038/ncb2883
Byrne P et al (2019) Statins for the primary prevention of cardiovascular disease: an overview of systematic reviews. BMJ open 9(4):e023085
pubmed: 31015265 pmcid: 6500096 doi: 10.1136/bmjopen-2018-023085
Lee MM et al (2019) Statins in the prevention and treatment of heart failure: a review of the evidence. Curr Atheroscler Rep 21(10):1–8
doi: 10.1007/s11883-019-0800-z
Korani S et al (2019) Parenteral systems for statin delivery: a review. Lipids Health Dis 18(1):1–9
doi: 10.1186/s12944-019-1139-8
De Angelis G (2004) The influence of statin characteristics on their safety and tolerability. Int J Clin Pract 58(10):945–955
pubmed: 15587774 doi: 10.1111/j.1368-5031.2004.00355.x
Liu J, Shen Q, Wu Y (2008) Simvastatin prevents cardiac hypertrophy in vitro and in vivo via JAK/STAT pathway. Life Sci 82(19–20):991–996
pubmed: 18400235 doi: 10.1016/j.lfs.2008.02.012
Climent E, Benaiges D, Pedro-Botet J (2021) Hydrophilic or lipophilic statins? Front Cardiovasc Med 8:491
doi: 10.3389/fcvm.2021.687585
Wang X, Chen J, Huang X (2019) Rosuvastatin Attenuates Myocardial Ischemia-Reperfusion Injury via Upregulating miR-17-3p-Mediated Autophagy. Cell Reprogram 21(6):323–330
pubmed: 31730378 pmcid: 6918854 doi: 10.1089/cell.2018.0053
Wolfrum S et al (2004) Simvastatin acutely reduces myocardial reperfusion injury in vivo by activating the phosphatidylinositide 3-kinase/Akt pathway. J Cardiovasc Pharmacol 44(3):348–355
pubmed: 15475833 doi: 10.1097/01.fjc.0000137162.14735.30
Rizvi SZH et al (2019) Simvastatin-loaded solid lipid nanoparticles for enhanced anti-hyperlipidemic activity in hyperlipidemia animal model. Int J Pharm 560:136–143
pubmed: 30753932 doi: 10.1016/j.ijpharm.2019.02.002
Luo K, Long, Xu B-c (2015) Reduced apoptosis after acute myocardial infarction by simvastatin. Cell Biochem Biophys 71(2):735–740
pubmed: 25304741 doi: 10.1007/s12013-014-0257-1
Nagaoka K et al (2015) A new therapeutic modality for acute myocardial infarction: nanoparticle-mediated delivery of pitavastatin induces cardioprotection from ischemia-reperfusion injury via activation of PI3K/Akt pathway and anti-inflammation in a rat model. PLoS ONE 10(7):e0132451
pubmed: 26167913 pmcid: 4500569 doi: 10.1371/journal.pone.0132451
Moghassemi S, Hadjizadeh A (2014) Nano-niosomes as nanoscale drug delivery systems: an illustrated review. J Controlled Release 185:22–36
doi: 10.1016/j.jconrel.2014.04.015
Naderi R et al (2021) Preparation and evaluation of crocin loaded in nanoniosomes and their effects on ischemia–reperfusion injuries in rat kidney. Sci Rep 11(1):1–12
doi: 10.1038/s41598-021-02073-w
Sharma A et al (2019) Niosomes: a promising approach in drug delivery systems. J Drug Delivery Ther 9(4):635–642
Naseroleslami M et al (2022) Simvastatin-loaded nano-niosomes confer cardioprotection against myocardial ischemia/reperfusion injury. Drug Delivery and Translational Research 12(6):1423–1432
pubmed: 34165730 doi: 10.1007/s13346-021-01019-z
He C et al (2010) Effects of particle size and surface charge on cellular uptake and biodistribution of polymeric nanoparticles. Biomaterials 31(13):3657–3666
pubmed: 20138662 doi: 10.1016/j.biomaterials.2010.01.065
Sharifi M et al (2021) Necroptosis and RhoA/ROCK pathways: molecular targets of Nesfatin-1 in cardioprotection against myocardial ischemia/reperfusion injury in a rat model. Mol Biol Rep 48(3):2507–2518
pubmed: 33755849 doi: 10.1007/s11033-021-06289-x
Rakhshan K et al (2019) ELABELA (ELA) peptide exerts cardioprotection against myocardial infarction by targeting oxidative stress and the improvement of heart function. Int J Pept Res Ther 25(2):613–621
doi: 10.1007/s10989-018-9707-8
Naseroleslami M et al (2020) Nesfatin-1 attenuates injury in a rat model of myocardial infarction by targeting autophagy, inflammation, and apoptosis. Archives of Physiology and Biochemistry, pp 1–9
Kheila M et al (2021) Human mesenchymal stem cells derived from amniotic membrane attenuate isoproterenol (ISO)-induced myocardial injury by targeting apoptosis. Med J Islamic Repub Iran 35:82
Firozian F et al (2020) Improvement of therapeutic potential N-acetylcysteine in acetaminophen hepatotoxicity by encapsulation in PEGylated nano-niosomes. Life Sci 255:117832
pubmed: 32450164 doi: 10.1016/j.lfs.2020.117832
Xu Y-Q et al (2016) Niosome encapsulation of curcumin: characterization and cytotoxic effect on ovarian cancer cells. Journal of Nanomaterials, 2016
Usman MRM, Ghuge PR, Jain BV (2017) Niosomes: a novel trend of drug delivery. Eur J Biomedical Pharm Sci 4(7):436–442
Verma A et al (2021) Emerging potential of niosomes in ocular delivery. Expert Opin Drug Deliv 18(1):55–71
pubmed: 32903034 doi: 10.1080/17425247.2020.1822322
Ge X et al (2019) Advances of non-ionic surfactant vesicles (niosomes) and their application in drug delivery. Pharmaceutics 11(2):55
pubmed: 30700021 pmcid: 6410054 doi: 10.3390/pharmaceutics11020055
Tuuminen R et al (2016) Simvastatin pretreatment reduces caspase-9 and RIPK1 protein activity in rat cardiac allograft ischemia-reperfusion. Transpl Immunol 37:40–45
pubmed: 27155462 doi: 10.1016/j.trim.2016.05.001
de Jesus Oliveira FM et al (2020) Simvastatin Posttreatment Controls Inflammation and Improves Bacterial Clearance in Experimental Sepsis. Mediators Inflamm, 2020: p. 1839762
Hadi NR et al (2013) Antiapoptotic effect of simvastatin ameliorates myocardial ischemia/reperfusion injury. International Scholarly Research Notices, 2013
Vilahur G et al (2009) Induction of RISK by HMG-CoA reductase inhibition affords cardioprotection after myocardial infarction. Atherosclerosis 206(1):95–101
pubmed: 19419716 doi: 10.1016/j.atherosclerosis.2009.02.009
Du Y et al (2018) Muscone improves cardiac function in mice after myocardial infarction by alleviating cardiac macrophage-mediated chronic inflammation through inhibition of NF-κB and NLRP3 inflammasome. Am J translational Res 10(12):4235
Qiao S et al (2021) Necrostatin-1 Analog DIMO Exerts Cardioprotective Effect against Ischemia Reperfusion Injury by Suppressing Necroptosis via Autophagic Pathway in Rats. Pharmacology 106(3–4):189–201
pubmed: 33621976 doi: 10.1159/000510864
Razavi Tousi SMT et al (2022) Mesenchymal Stem Cells Derived from Human Amniotic Membrane Increase VEGF and Extenuate Fibrosis in Heart Failure Rats.Iranian Journal of Science and Technology, Transactions A: Science, : p.1–11
Bai R et al (2017) Corydalis hendersonii Hemsl. protects against myocardial injury by attenuating inflammation and fibrosis via NF-κB and JAK2-STAT3 signaling pathways. J Ethnopharmacol 207:174–183
pubmed: 28629818 doi: 10.1016/j.jep.2017.06.020
Wang X et al (2022) Simvastatin Combined with Resistance Training Improves Outcomes in Patients with Chronic Heart Failure by Modulating Mitochondrial Membrane Potential and the Janus Kinase/Signal Transducer and Activator of Transcription 3 Signaling Pathways. Cardiovasc Ther, 2022: p. 8430733
Zhang J et al (2005) Simvastatin regulates myocardial cytokine expression and improves ventricular remodeling in rats after acute myocardial infarction. Cardiovasc Drugs Ther 19(1):13–21
pubmed: 15883752 doi: 10.1007/s10557-005-6893-3
Garg S, Bhattia J (2018) Fisetin, a PPAR gamma agonist improves myocardial injury in rats through Inhibition of MAPK Signalling Pathway mediated oxidative stress and inflammation in Experimental Model of Myocardial Ischemia Reperfusion Injury. in Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (The 18th World Congress of Basic and Clinical Pharmacology). Japanese Pharmacological Society
Zhou QL et al (2018) FPR1 gene silencing suppresses cardiomyocyte apoptosis and ventricular remodeling in rats with ischemia/reperfusion injury through the inhibition of MAPK signaling pathway. Exp Cell Res 370(2):506–518
pubmed: 30031130 doi: 10.1016/j.yexcr.2018.07.016
Xu L et al (2022) Simvastatin inhibits the inflammation and oxidative stress of human neutrophils in sepsis via autophagy induction.Mol Med Rep, 25(1)
Hua Y et al (2018) Evaluation of effect of atorvastatin on left ventricular systolic function in rats with myocardial infarction via 2D-STI technique. Experimental and Therapeutic Medicine 15(5):4386–4394 .Statements & Declarations
pubmed: 29725379 pmcid: 5920387

Auteurs

Maryam Naseroleslami (M)

Department of Cellular and Molecular Biology, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.

Masoomeh Sharifi (M)

Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Neda Mousavi Niri (N)

Department of Medical Biotechnology, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.

Nahid Aboutaleb (N)

Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran. Aboutaleb.n@iums.ac.ir.
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Aboutaleb.n@iums.ac.ir.

Articles similaires

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male
Humans Meals Time Factors Female Adult

Classifications MeSH