ArticleBiochemical and biophysical research communications2018
Post-ischemic administration of 5-methoxyindole-2-carboxylic acid at the onset of reperfusion affords neuroprotection against stroke injury by preserving mitochondrial function and attenuating oxidative stress.
Article in Biochemical and biophysical research communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 32 citations in OpenAlex.
- Renoprotection by 5-Methoxytryptophan in Kidney Disease.Biomolecules · 2026Review
- Exploring genetic associations and drug targets for mitochondrial proteins and schizophrenia risk.Schizophrenia (Heidelberg, Germany) · 2025Article
- Discovery of a New Polymorph of 5-Methoxy-1Molecules (Basel, Switzerland) · 2024Article
- Roles of Dihydrolipoamide Dehydrogenase in Health and Disease.Antioxidants & redox signaling · 2023Review
- Emerging Roles of NDUFS8 Located in Mitochondrial Complex I in Different Diseases.Molecules (Basel, Switzerland) · 2022Review
- Para‑hydroxybenzaldehyde against transient focal cerebral ischemia in rats via mitochondrial preservation.Experimental and therapeutic medicine · 2022Article
- Biological Implications of a Stroke Therapy Based in Neuroglobin Hyaluronate Nanoparticles. Neuroprotective Role and Molecular Bases.International journal of molecular sciences · 2021Article
- Cadmium-Induced Kidney Injury: Oxidative Damage as a Unifying Mechanism.Biomolecules · 2021Review
- Surface-modified engineered exosomes attenuated cerebral ischemia/reperfusion injury by targeting the delivery of quercetin towards impaired neurons.Journal of nanobiotechnology · 2021Article
- Oxidative Stress at the Crossroads of Aging, Stroke and Depression.Aging and disease · 2020Review
- 5-Methoxyindole-2-Carboylic Acid (MICA) Fails to Retard Development and Progression of Type II Diabetes in ZSF1 Diabetic Rats.Reactive oxygen species (Apex, N.C.) · 2020Article
- Chronic Inhibition of Mitochondrial Dihydrolipoamide Dehydrogenase (DLDH) as an Approach to Managing Diabetic Oxidative Stress.Antioxidants (Basel, Switzerland) · 2019Article
- Critical Role of Nrf2 in Experimental Ischemic Stroke.Frontiers in pharmacology · 2019Review
- Reexploring 5-methoxyindole-2-carboxylic acid (MICA) as a potential antidiabetic agent.Diabetes, metabolic syndrome and obesity : targets and therapy · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
We previously reported that 5-methoxyindole-2-carboxylic acid (MICA) could induce preconditioning effect in the ischemic brain of rat. In the present study, we addressed the question of whether MICA could also trigger a postconditioning effect in ischemic stroke. To this end, MICA (100 mg/kg body weight) was injected intraperitoneally at the onset of 24 h reperfusion following 1 h ischemia in rat brain. Results indicate that stroked animals treated with MICA showed less brain infarction volume than that of vehicle-treated animals. Further experiments revealed that brain mitochondrial complexes I and IV showed elevated enzymatic activities in MICA treated group and the elevation in complex I activity was likely contributed by seemingly enhanced expression of many complex I subunits, which was determined by mass spectral peptide sequencing. When compared with vehicle-treated rats, the preservation of complexes I and IV activities was shown to be accompanied by enhanced mitochondrial membrane potential, increased ATP production, and decreased caspase-3 activity. Additional studies also indicate the involvement of NQO1 upregulation by the Nrf2 signaling pathway in this MICA postconditioning paradigm. Consequently, attenuated oxidative stress in the MICA treated group reflected by decrease in H
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.