ArticleArchives of toxicology2015
Tetramethylpyrazine (TMP) protects against sodium arsenite-induced nephrotoxicity by suppressing ROS production, mitochondrial dysfunction, pro-inflammatory signaling pathways and programed cell death.
Article in Archives of toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 3 of them syntheses that pooled it.
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Who cites it
47 citing papers in PubMed, 3 syntheses or guidelines pooled it, 96 citations in OpenAlex.
- Meta-analysis of TLR4 pathway-related protein alterations induced by arsenic exposure.Biological trace element research · 2023Pooled it
- A Systematic Review of the Various Effect of Arsenic on Glutathione Synthesis In Vitro and In Vivo.BioMed research international · 2020Pooled it
- Divergent Effects of Arsenic on NF-κB Signaling in Different Cells or Tissues: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2016Pooled it
- Metal mechanisms of mitochondrial toxicity: recent review of arsenic, cadmium, and lead-induced nephrotoxicity.Environmental science and pollution research international · 2025Review
- Protective Effects of Lactoferrin Treatment Against Sodium Arsenite Exposure-Induced Nephrotoxicity.Biological trace element research · 2025Article
- Nephroprotective effects of substances of medicine food homology and traditional Chinese medicine phytochemicals against acute kidney injury.Frontiers in pharmacology · 2025Review
- Tetramethylpyrazine attenuates sodium arsenite-induced acute kidney injury by improving the autophagic flux blockade via a YAP1-Nrf2-p62-dependent mechanism.International journal of biological sciences · 2025Article
- Risk assessment of heavy metal toxicity induced by platinum accumulation in tumor patients.PeerJ · 2025Article
- Cannabidiol attenuates arsenic-induced nephrotoxicityResearch in pharmaceutical sciences · 2024Article
- Tetramethylpyrazine attenuates renal tubular epithelial cell ferroptosis in contrast-induced nephropathy by inhibiting transferrin receptor and intracellular reactive oxygen species.Clinical science (London, England : 1979) · 2024Article
- Pharmacokinetics, Safety Profile, and Tolerability of Tetramethylpyrazine Nitrone Tablets After Single and Multiple Ascending Doses in Healthy Chinese Volunteers.European journal of drug metabolism and pharmacokinetics · 2024Article
- Recent insights into autophagy and metals/nanoparticles exposure.Toxicological research · 2023Review
- Tyrosol and Olive Oil Ameliorate Sodium Arsenate-Induced Nephrotoxicity by Modulating of Oxidative Stress and Histological Changes in Mice.International journal of preventive medicine · 2023Article
- Nephroprotective Effects of Selenium Nanoparticles Against Sodium Arsenite-Induced Damages.International journal of nanomedicine · 2023Article
- Potential therapeutic effects of Chinese meteria medica in mitigating drug-induced acute kidney injury.Frontiers in pharmacology · 2023Review
- Role of ACSL4 in the chemical-induced cell death in human proximal tubule epithelial HK-2 cells.Bioscience reports · 2022Article
- Tetramethylpyrazine: An Active Ingredient of Chinese Herbal Medicine With Therapeutic Potential in Acute Kidney Injury and Renal Fibrosis.Frontiers in pharmacology · 2022Review
- Article
- Efficacy and Safety of Chuan Huang Fang Combining Reduced Glutathione in Treating Acute Kidney Injury (Grades 1-2) on Chronic Kidney Disease (Stages 2-4): Study Protocol for a Multicenter Randomized Controlled Clinical Trial.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Protective Effect ofMolecules (Basel, Switzerland) · 2021Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Although kidney is a target organ of arsenic cytotoxicity, the underlying mechanisms of arsenic-induced nephrotoxicity remain poorly understood. As tetramethylpyrazine (TMP) has recently been found to be a renal protectant in multiple kidney injuries, we hypothesize that TMP could suppress arsenic nephrotoxicity. In this study, human renal proximal tubular epithelial cell line HK-2 was used to elucidate the precise mechanisms of arsenic nephrotoxicity as well as the protective mechanism of TMP in these cells. Sodium arsenite exposure dramatically increased cellular reactive oxygen species (ROS) production, decreased levels of cellular glutathione (GSH), decreased cytochrome c oxidase activity and mitochondrial membrane potential, which indicated mitochondrial dysfunction. On the other hand, sodium arsenite activated pro-inflammatory signals, including β-catenin, nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (MAPK), tumor necrosis factor alpha and cyclooxygenase-2 (COX-2). Small molecule inhibitors of NF-κB and p38 MAPK blocked arsenic-induced COX-2 expression, suggesting arsenic-induced COX-2 up-regulation was NF-κB- and p38 MAPK-dependent. Finally, sodium arsenite induced autophagy in HK-2 cells at early phase (6 h) and the subsequent apoptosis at 24 h. Treatment by TMP or by the antioxidant N-acetylcysteine decreased arsenic-induced ROS production, enhanced GSH levels, prevented mitochondria dysfunction and suppressed the activation of pro-inflammatory signals and the development of autophagy and apoptosis. Our results suggested that TMP may be used as a new potential therapeutic agent to prevent arsenic-induced nephrotoxicity by suppressing these pathological processes.
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