Molecular Mechanisms of the Neuroprotective Effect of Methylene Blue

Gureev, Artem P.; Sadovnikova, Irina S.; Popov, Vasily N.

doi:10.1134/s0006297922090073

Cited by 22 publications

(10 citation statements)

References 130 publications

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“…The various strategies used to prevent cisplatin-induced nephrotoxicity are actively studied; for example, hydration with magnesium and mannitol supplements [ 41 ], the use of various natural and synthetic antioxidants [ 42 ], nitric oxide modulators, diuretics, and cytoprotective and anti-apoptotic agents [ 43 , 44 ] such as cilastatin [ 45 , 46 ], vincamine [ 47 ], dibenzazepine [ 48 ], astaxanthin [ 49 ], theophylline [ 50 ], and others. It is known that methylene blue has a wide spectrum of action, including cytoprotective, anti-apoptotic, and antioxidant actions [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Methylene Blue Induces Antioxidant Defense and Reparation of Mitochondrial DNA in a Nrf2-Dependent Manner during Cisplatin-Induced Renal Toxicity

Samoylova

Gureev

Popov

2023

IJMS

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Cisplatin is a platinum-based cytostatic drug that is widely used for cancer treatment. Mitochondria and mtDNA are important targets for platinum-based cytostatics, which mediates its nephrotoxicity. It is important to develop therapeutic approaches to protect the kidneys from cisplatin during chemotherapy. We showed that the exposure of mitochondria to cisplatin increased the level of lipid peroxidation products in the in vitro experiment. Cisplatin caused strong damage to renal mtDNA, both in the in vivo and in vitro experiments. Cisplatin injections induced oxidative stress by depleting renal antioxidants at the transcriptome level but did not increase the rate of H2O2 production in isolated mitochondria. Methylene blue, on the contrary, induced mitochondrial H2O2 production. We supposed that methylene blue-induced H2O2 production led to activation of the Nrf2/ARE signaling pathway. The consequences of activation of this signaling pathway were manifested in an increase in the expression of some antioxidant genes, which likely caused a decrease in the amount of mtDNA damage. Methylene blue treatment induced an increase in the expression of genes that were involved in the base excision repair (BER) pathway: the main pathway for mtDNA reparation. It is known that the expression of these genes can also be regulated by the Nrf2/ARE signaling pathway. We can assume that the protective effect of methylene blue is related to the activation of Nrf2/ARE signaling pathways, which can activate the expression of genes related to antioxidant defense and mtDNA reparation. Thus, the protection of kidney mitochondria from cisplatin-induced damage using methylene blue can significantly expand its application in medicine.

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Section: Discussionmentioning

confidence: 99%

Methylene Blue Induces Antioxidant Defense and Reparation of Mitochondrial DNA in a Nrf2-Dependent Manner during Cisplatin-Induced Renal Toxicity

Samoylova

Gureev

Popov

2023

IJMS

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“…The histologic investigation of these bundles revealed them to be autonomous nerve fibers [ 20 ]. Additionally, methylene blue has emerged as a potential drug in the treatment of neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, traumatic brain injury, etc., owing to its cognitive improvement and neuroprotective functions [ 32 , 33 ]. These functions are based on the anti-oxidative and anti-inflammatory effects of MB, and its ability to prevent autophagy [ 34 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

Functional Recovery after the Application of Amniotic Tissues and Methylene Blue during Radical Prostatectomy—A Pilot Study

et al. 2023

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Amniotic tissues and methylene blue (MB) provide the ability for neuroregeneration, and MB enables intraoperative neurostaining. We first combined the techniques to explore a neuroprotective effect on early functional outcomes in a retrospective proof-of-concept trial of 14 patients undergoing radical prostatectomy (RP). The patients were followed up at a median of 13 months, and the continence and potency rates were reported. Early recovery of continence was found after three months. No effect on potency was detected. The findings indicate the feasibility of this tissue-engineering strategy, and justify prospective comparative studies.

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“…Apart from stabilizing the SOD1 dimer and promoting proper folding to prevent SOD1 aggregation, molecules which can interfere with the self-assembly, the nucleation, or the fibrillation process are of high therapeutic interest. A prime example is Methylene Blue (MB), a phenothiazine dye, which has shown considerable potential in modulating the aggregation of various amyloidogenic proteins (Gureev et al, 2022). The ability of MB to readily cross the bloodbrain barrier has significantly increased interest in its use as a therapeutic agent for central nervous system disorders (Rojas et al, 2012).…”

Section: Inhibiting Self-assembly and The Aggregation Processmentioning

confidence: 99%

Protein aggregation and therapeutic strategies in SOD1- and TDP-43- linked ALS

Tsekrekou,

Giannakou,

Papanikolopoulou

et al. 2024

Front. Mol. Biosci.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with severe socio-economic impact. A hallmark of ALS pathology is the presence of aberrant cytoplasmic inclusions composed of misfolded and aggregated proteins, including both wild-type and mutant forms. This review highlights the critical role of misfolded protein species in ALS pathogenesis, particularly focusing on Cu/Zn superoxide dismutase (SOD1) and TAR DNA-binding protein 43 (TDP-43), and emphasizes the urgent need for innovative therapeutic strategies targeting these misfolded proteins directly. Despite significant advancements in understanding ALS mechanisms, the disease remains incurable, with current treatments offering limited clinical benefits. Through a comprehensive analysis, the review focuses on the direct modulation of the misfolded proteins and presents recent discoveries in small molecules and peptides that inhibit SOD1 and TDP-43 aggregation, underscoring their potential as effective treatments to modify disease progression and improve clinical outcomes.

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Molecular Mechanisms of the Neuroprotective Effect of Methylene Blue

Cited by 22 publications

References 130 publications

Methylene Blue Induces Antioxidant Defense and Reparation of Mitochondrial DNA in a Nrf2-Dependent Manner during Cisplatin-Induced Renal Toxicity

Methylene Blue Induces Antioxidant Defense and Reparation of Mitochondrial DNA in a Nrf2-Dependent Manner during Cisplatin-Induced Renal Toxicity

Functional Recovery after the Application of Amniotic Tissues and Methylene Blue during Radical Prostatectomy—A Pilot Study

Protein aggregation and therapeutic strategies in SOD1- and TDP-43- linked ALS

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