ArticleJournal of cellular physiology2018
Tetrahydrocurcumin ameliorates homocysteine-mediated mitochondrial remodeling in brain endothelial cells.
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Homocysteine and mitophagy in diabetic retinopathy: unraveling the underlying molecular crosstalk.Endocrine · 2026Review
- Etomidate Prevents Homocysteine‑Induced Endothelial Dysfunction by Suppressing PERK‑eIF2α‑ATF4 Signaling, Oxidative Stress, Mitochondrial Injury, and Autophagic Dysregulation.Journal of biochemical and molecular toxicology · 2026Article
- Differential Effects of Turmeric Bioactive Compounds on Neuroinflammation and Mitochondrial Homeostasis in Brain Regions in a Rodent Model of Neuropathic Pain.Metabolites · 2026Article
- Hyperhomocysteinemia Induced Mitochondrial Dysfunction Disrupting the Eye Development.Neurotoxicity research · 2025Article
- Curcumin improves diabetic vascular aging rats and high glucose-induced cells aging by promoting mitophagy.3 Biotech · 2025Article
- Influence of homocysteine on regulating immunothrombosis: mechanisms and therapeutic potential in management of infections.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023Review
- Article
- Xiaojianzhong decoction prevents gastric precancerous lesions in rats by inhibiting autophagy and glycolysis in gastric mucosal cells.World journal of gastrointestinal oncology · 2023Article
- The multifaceted roles of natural products in mitochondrial dysfunction.Frontiers in pharmacology · 2023Review
- Tetrahydrocurcumin-Related Vascular Protection: An Overview of the Findings from Animal Disease Models.Molecules (Basel, Switzerland) · 2022Review
- Article
- Increased homocysteine regulated by androgen activates autophagy by suppressing the mammalian target of rapamycin pathway in the granulosa cells of polycystic ovary syndrome mice.Bioengineered · 2022Article
- Mitochondrial-Respiration-Improving Effects of Three Different Gardeniae Fructus Preparations and Their Components.ACS omega · 2021Article
- Mitochonic acid 5 regulates mitofusin 2 to protect microglia.Neural regeneration research · 2021Article
- Natural products targeting mitochondria: emerging therapeutics for age-associated neurological disorders.Pharmacology & therapeutics · 2021Review
- Preliminary analysis of immunoregulatory mechanism of hyperhomocysteinemia-induced brain injury in Wistar-Kyoto rats.Experimental and therapeutic medicine · 2021Article
- Exosomal lncRNA-H19 promotes osteogenesis and angiogenesis through mediating Angpt1/Tie2-NO signaling in CBS-heterozygous mice.Theranostics · 2021Article
- Homocysteine and Mitochondria in Cardiovascular and Cerebrovascular Systems.International journal of molecular sciences · 2020Review
- Folic Acid Decreases Astrocyte Apoptosis by Preventing Oxidative Stress-Induced Telomere Attrition.International journal of molecular sciences · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Homocysteine (Hcy) causes endothelial dysfunction by inducing oxidative stress in most neurodegenerative disorders. This dysfunction is highly correlated with mitochondrial dynamics such as fusion and fission. However, there are no strategies to prevent Hcy-induced mitochondrial remodeling. Tetrahydrocurcumin (THC) is an anti-inflammatory and anti-oxidant compound. We hypothesized that THC may ameliorates Hcy-induced mitochondria remodeling in mouse brain endothelial cells (bEnd3) cells. bEnd3 cells were exposed to Hcy treatment in the presence or absence of THC. Cell viability and autophagic cell death were measured with MTT and MDC staining assay. Reactive oxygen species (ROS) production was determined using DCFH-DA staining by confocal microscopy. Autophagy flux was assessed using a conventional GFP-microtubule-associated protein 1 light chain 3 (LC3) dot assay. Interaction of phagophore marker LC-3 with mitochondrial receptor NIX was observed by confocal imaging. Mitochondrial fusion and fission were evaluated by western blot and RT-PCR. Our results demonstrated that Hcy resulted in cell toxicity in a dose-dependent manner and supplementation of THC prevented the detrimental effects of Hcy on cell survival. Furthermore, Hcy also upregulated fission marker (DRP-1), fusion marker (Mfn2), and autophagy marker (LC-3). Finally, we observed that Hcy activated mitochondrial specific phagophore marker (LC-3) and co-localized with the mitochondrial receptor NIX, as viewed by confocal microscopy. Pretreatment of bEnd3 with THC (15 μM) ameliorated Hcy-induced oxidative damage, mitochondrial fission/fusion, and mitophagy. Our studies strongly suggest that THC has beneficial effects on mitochondrial remodeling and could be developed as a potential therapeutic agent against hyperhomocysteinemia (HHcy) induced mitochondrial dysfunction.
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Registered trials
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