Cited by 27Mangiferin and Mango ExtractsFluoride Effects and RemovalHeavy Metal Exposure and Toxicity

Mangiferin prevents the impairment of mitochondrial dynamics and an increase in oxidative stress caused by excessive fluoride in SH‐SY5Y cells

Tang, Zhi, Lai, Chen‐Cen, Luo, Jun, Ding, Yuan‐Ting, Chen, Qian, Guan, Zhi‐Zhong·2021·Journal of Biochemical and Molecular Toxicology

Abstract

Previous studies both invivo and in vitro have revealed that high levels of fluoride cause neurotoxicity. Mangiferin has been reported to possess antioxidant, antiapoptotic, and anti-inflammatory properties. The present study was designed to characterize the mechanisms by which mangiferin protects against NaF-induced neurotoxicity. Increased levels of proapoptotic Bax, Caspase-3, Caspase-9, and cleaved-caspase 3, as well as a decreased level of antiapoptotic Bcl-2 induced by fluoride in human neuroblastoma SH-SY5Y cells, these effects were prevented by pretreatment of mangiferin. In addition, mangiferin attenuated the enhancement of p-JNK, reductions of Nrf2 and HO-1, and increased level of the mitochondrial fission proteins Drp1 caused by fluoride. Moreover, oxidative stress, as reflected in the levels of reactive oxygen species, 8-hydroxy-2'-deoxyguanosine, and 4-hydroxynonenal, was elevated by fluoride and these effects were again ameliorated by mangiferin. In conclusion, protection by mangiferin against fluoride-induced neurotoxicity involves normalizing the impaired mitochondrial apoptotic pathway and dynamics and reducing oxidative stress via inactivation of the JNK and activation of the Nrf2/HO-1 pathways.

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Crossref · 10.1002/jbt.22705

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  • In models of fluoride-induced neurotoxicity, MGF restores mitochondrial integrity by inhibiting proapoptotic proteins (Bax, caspase-3 and caspase-9) and upregulating Bcl-2.

    “Notably, in models of fluoride-induced neurotoxicity, MGF restores mitochondrial integrity by inhibiting proapoptotic proteins (Bax, caspase-3 and caspase-9) and upregulating Bcl-2.”
  • The protective effects of MGF in fluoride-induced neurotoxicity are mediated via JNK inhibition and activation of the Nrf2/HO-1 pathway.

    “These protective effects are mediated via JNK inhibition and activation of the Nrf2/HO-1 pathway (71).”

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Authors
Tang, Z., Lai, C., Luo, J., Ding, Y., Chen, Q., & Guan, Z.
Affiliations
  • Guiyang Medical University (CN)
  • Clinical Research Center The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine Guiyang China
  • Guizhou University (CN)
Corresponding author
Guan, Zhi‐Zhong
Venue
Journal of Biochemical and Molecular Toxicology
Publisher
Wiley
Published
2021-01-04
Volume
35
Issue
4
Pages
e22705-e22705
ISSN
  • 0887-2082 (ISSN-L)
  • 1095-6670
  • 1099-0461
OpenAlex
W3120942908
Cited by
26
References
39
Citations by year
2026: 2 · 2025: 6 · 2024: 5 · 2023: 5 · 2022: 8
FWCI
5.06
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Biochemical and Molecular Toxicology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Guizhou Science and Technology Department ([2018]1009, [2018]2772, LH [2017]7156, [2017]1014, [2018]5752)
  • Science and Technology Bureau, Guiyang Municipal Government ([2019]9‐2‐11, [2019]9‐2‐7)
  • National Natural Science Foundation of China (81560241, 81960265, U1812403)
  • Department of Education of Guizhou Province (KY [2016]035, [2018]214)
Topics
  • Health Sciences › Medicine › Complementary and alternative medicine › Mangiferin and Mango Extracts
  • Physical Sciences › Environmental Science › Water Science and Technology › Fluoride Effects and Removal
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
Keywords
mangiferin, fluoride neurotoxicity, mitochondrial dynamics, mitochondrial fission, oxidative stress, apoptosis, JNK signaling, Nrf2/HO-1 pathway, Drp1, SH-SY5Y cells, reactive oxygen species, neuroprotection
MeSH terms
Fluorides, Humans, Mitochondria, Neoplasm Proteins, Neuroblastoma, Oxidative Stress, Xanthones, Cell Line, Tumor, Apoptosis Regulatory Proteins

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