ArticleCellular and molecular neurobiology2014
Investigating the protective effect of lithium against high glucose-induced neurotoxicity in PC12 cells: involvements of ROS, JNK and P38 MAPKs, and apoptotic mitochondria pathway.
Article in Cellular and molecular neurobiology, 2014. 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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22 citing papers in PubMed, 44 citations in OpenAlex.
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- Microdose Lithium Protects against Pancreatic Islet Destruction and Renal Impairment in Streptozotocin-Elicited Diabetes.Antioxidants (Basel, Switzerland) · 2021Article
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- Protective effects of atorvastatin on high glucose-induced oxidative stress and mitochondrial apoptotic signaling pathways in cultured chondrocytes.Journal of physiology and biochemistry · 2019Article
- Phosphodiesterase 4 and 7 inhibitors produce protective effects against high glucose-induced neurotoxicity in PC12 cells via modulation of the oxidative stress, apoptosis and inflammation pathways.Metabolic brain disease · 2018Article
- Selenocysteine antagonizes oxygen glucose deprivation-induced damage to hippocampal neurons.Neural regeneration research · 2018Article
- Protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α, VEGF and p38 MAPK signaling pathwayExperimental and therapeutic medicine · 2018Article
- Neonatal hyperglycemia induces cell death in the rat brain.Metabolic brain disease · 2018Article
- Cellular death, reactive oxygen species (ROS) and diabetic complications.Cell death & disease · 2018Review
- Inhibition of ROS-mediated activation Src-MAPK/AKT signaling by orientin alleviates HDrug design, development and therapy · 2018Article
- Erythropoietin ameliorates diabetes-associated cognitive dysfunction in vitro and in vivo.Scientific reports · 2017Article
- Studying neuroprotective effect of Atorvastatin as a small molecule drug on high glucose-induced neurotoxicity in undifferentiated PC12 cells: role of NADPH oxidase.Metabolic brain disease · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia that occurs under the diabetic condition is a major cause of diabetic complications such as diabetic neuropathy, one of the most common diabetes-related complications. It is well known that hyperglycemia could result in generation of reactive oxygen species (ROS). Over production of ROS recommended as an important mediator for apoptotic signaling pathway as well as a key early event in the development of diabetic neuropathy. Recently, many studies have indicated that lithium has robust neuroprotective effect in relation to several neurodegenerative diseases. The present study aimed to examine effects of lithium on high glucose (HG)-induced neurotoxicity and to determine some of the underlying molecular mechanisms involved in this response in PC12 cells as a neuronal culture model for diabetic neuropathy. PC12 cells were pretreated with different concentrations of lithium for 7 days, exposed to HG for 24 h. Cell viability was measured by MTT assay. ROS and lipid peroxidation levels as well as superoxide dismutase activity were measured. In order to examine the underlying molecular mechanisms, the expressions of Bax, Bcl-2, Caspase-3, total and phosphorylated JNK and P38 MAPK were also analyzed by Western blotting. The present results indicated that pretreatment with 1 mM lithium has protected PC12 cells against HG-induced apoptotic cell death. It could reduce ROS generation, Bax/Bcl-2 ratio, Caspase-3 activation, and JNK and P38 MAPK phosphorylation. It may be concluded that in HG condition, lithium pretreatment could prevent mitochondrial apoptosis as well as JNK and P38 MAPK pathway in PC12 cells.
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