ArticleOxidative medicine and cellular longevity2016
t-BHQ Provides Protection against Lead Neurotoxicity via Nrf2/HO-1 Pathway.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 74 citations in OpenAlex.
- Fermentation Status Dictates Organ-Selective Protection of a Millet-Based Dairy Beverage Against Sub-Chronic Lead Toxicity in Rats.Biological trace element research · 2026Article
- Nrf2 Activation Alleviates Silica-Induced Toxicity in Alveolar Macrophages via Glutamine Metabolic Reprogramming.Toxics · 2026Article
- The effect of tert-butylhydroquinone on anxiolytic- and antidepressant-like behaviors induced by post-traumatic stress disorder: A behavioral and molecular study.Iranian journal of basic medical sciences · 2026Article
- Dimethyl fumarate therapy in a Western diet pregnancy model: a pilot study in guinea pigs.PeerJ · 2026Article
- Identification and Validation of Endoplasmic Reticulum Stress-Related Gene in Traumatic Brain Injury.Journal of molecular neuroscience : MN · 2024Article
- Butylphthalide inhibits ferroptosis and ameliorates cerebral Ischaemia-Reperfusion injury in rats by activating the Nrf2/HO-1 signalling pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Review
- Protective effect of luteoloside against Toxoplasma gondii-induced liver injury through inhibiting TLR4/NF-κB and P2X7R/NLRP3 and enhancing Nrf2/HO-1 signaling pathway.Parasitology research · 2023Article
- Iron homeostasis and post-hemorrhagic hydrocephalus: a review.Frontiers in neurology · 2023Review
- Molecular mechanisms and therapeutic effects of different vitamins and minerals in COVID-19 patients.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2022Review
- Diosmetin Protects against Cardiac Hypertrophy via p62/Keap1/Nrf2 Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- N,N'bis-(2-mercaptoethyl) isophthalamide (NBMI) exerts neuroprotection against lead-induced toxicity in U-87 MG cells.Archives of toxicology · 2021Article
- MOLECULAR MECHANISMS OF LEAD NEUROTOXICITY.Advances in neurotoxicology · 2021Article
- Oxidative Stress as a Common Key Event in Developmental Neurotoxicity.Oxidative medicine and cellular longevity · 2021Review
- Promoting Nrf2/Sirt3-Dependent Mitophagy Suppresses Apoptosis in Nucleus Pulposus Cells and Protects against Intervertebral Disc Degeneration.Oxidative medicine and cellular longevity · 2021Article
- Protective Role of Nrf2 in Renal Disease.Antioxidants (Basel, Switzerland) · 2020Review
- (+)-Usnic Acid Induces ROS-dependent Apoptosis via Inhibition of Mitochondria Respiratory Chain Complexes and Nrf2 Expression in Lung Squamous Cell Carcinoma.International journal of molecular sciences · 2020Article
- Umbelliferone Inhibits Spermatogenic Defects and Testicular Injury in Lead-Intoxicated Rats by Suppressing Oxidative Stress and Inflammation, and Improving Nrf2/HO-1 Signaling.Drug design, development and therapy · 2020Article
- Isoflurane Postconditioning Upregulates Phosphorylated Connexin 43 in the Middle Cerebral Artery Occlusion Model and Is Probably Associated with the TGF-BioMed research international · 2020Article
- A Novel STAT3-Mediated GATA6 Pathway Contributes toOxidative medicine and cellular longevity · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neurotoxicity of lead has been well established, and oxidative stress is strongly associated with lead-induced neurotoxicity. Nrf2 is important for protection against oxidative stress in many disease models. We applied t-BHQ, which is an Nrf2 activator, to investigate the possible role of Nrf2 in the protection against lead neurotoxicity. t-BHQ significantly attenuated the oxidative stress in developmental rats by decreasing MDA level, as well as by increasing SOD activity and GSH content, in the hippocampus and frontal cortex. Furthermore, neuronal apoptosis was detected by Nissl staining, and Bax expression was inhibited in the t-BHQ-treated group. Results showed that t-BHQ suppressed ROS production and caspase 3/7 activity but increased intracellular GSH content, in SH-SY5Y cells under lead exposure. Moreover, in vivo and in vitro, t-BHQ enhanced the nuclear translocation of Nrf2 and binding to ARE areas but did not induce Nrf2 transcription. These phenomena were confirmed using RT-PCR, EMSA, Western blot, and immunofluorescence analyses. Subsequent upregulation of the expression of HO-1, NQO1, and GCLC was observed. However, knockdown of Nrf2 or HO-1 adversely affected the protective effects of t-BHQ against lead toxicity in SH-SY5Y cells. Thus, t-BHQ can protect against lead neurotoxicity, depending on the Nrf2/HO-1 pathway.
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