title: Curcumin alleviates oxidative stress and mitochondrial dysfunction in astrocytes.
abstract: Oxidative stress plays a critical role in various neurodegenerative diseases, thus alleviating oxidative stress is a potential strategy for therapeutic intervention and/or prevention of neurodegenerative diseases. In the present study, alleviation of oxidative stress through curcumin is investigated in A172 (human glioblastoma cell line) and HA-sp (human astrocytes cell line derived from the spinal cord) astrocytes. H2O2 was used to induce oxidative stress in astrocytes (A172 and HA-sp). Data show that H2O2 induces activation of astrocytes in dose- and time-dependent manner as evident by increased expression of GFAP in A172 and HA-sp cells after 24 and 12h respectively. An upregulation of Prdx6 was also observed in A172 and HA-sp cells after 24h of H2O2 treatment as compared to untreated control. Our data also showed that curcumin inhibits oxidative stress-induced cytoskeleton disarrangement, and impedes the activation of astrocytes by inhibiting upregulation of GFAP, vimentin and Prdx6. In addition, we observed an inhibition of oxidative stress-induced inflammation, apoptosis and mitochondria fragmentation after curcumin treatment. Therefore, our results suggest that curcumin not only protects astrocytes from H2O2-induced oxidative stress but also reverses the mitochondrial damage and dysfunction induced by oxidative stress. This study also provides evidence for protective role of curcumin on astrocytes by showing its effects on attenuating reactive astrogliosis and inhibiting apoptosis.
authors.affiliation: Department of Surgery, Division of Neurosurgery, University of Nebraska Medical Center, Omaha, NE, USA.
authors.forename: Amita
authors.initials: A
authors.lastname: Daverey
authors.affiliation: Department of Surgery, Division of Neurosurgery, University of Nebraska Medical Center, Omaha, NE, USA. Electronic address: agrawals@unmc.edu.
authors.forename: Sandeep K
authors.initials: SK
authors.lastname: Agrawal
mesh_terms: D000975:Antioxidants / Q000494:pharmacology* / Q000633:toxicity; D001253:Astrocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D015153:Blotting, Western; D020170:Caspase 1 / Q000378:metabolism; D002460:Cell Line; D003474:Curcumin / Q000494:pharmacology* / Q000633:toxicity; D005455:Fluorescent Antibody Technique; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006861:Hydrogen Peroxide; D018613:Microscopy, Confocal; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D063306:Mitophagy / Q000187:drug effects / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D054465:Peroxiredoxin VI / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology* / Q000633:toxicity
chemical_list: D000975:Antioxidants; D005904:Glial Fibrillary Acidic Protein; D020011:Protective Agents; D006861:Hydrogen Peroxide; C515977:PRDX6 protein, human; D054465:Peroxiredoxin VI; D020170:Caspase 1; D003474:Curcumin
keywords: GFAP; astrocytes; curcumin; neurodegenerative diseases; oxidative stress