Evaluating the Protective Effects of Thymoquinone on Methamphetamine-induced Toxicity in an In Vitro Model Based on Differentiated PC12 Cells.
Seyed Mobin Seyed AliyanAli RoohbakhshMarzieh Jafari FakhrabadZahar SalmasiMohammad MoshiriNiosha ShahbaziLeila EtemadPublished in: Alternatives to laboratory animals : ATLA (2024)
Methamphetamine (Meth) is a highly addictive stimulant. Its potential neurotoxic effects are mediated through various mechanisms, including oxidative stress and the initiation of the apoptotic process. Thymoquinone (TQ), obtained from Nigella sativa seed oil, has extensive antioxidant and anti-apoptotic properties. This study aimed to investigate the potential protective effects of TQ against Meth-induced toxicity by using an in vitro model based on nerve growth factor-differentiated PC12 cells. Cell differentiation was assessed by detecting the presence of a neuronal marker with flow cytometry. The effects of Meth exposure were evaluated in the in vitro neuronal cell-based model via the determination of cell viability (in an MTT assay) and apoptosis (by annexin/propidium iodide staining). The generation of reactive oxygen species (ROS), as well as the levels of glutathione (GSH) and dopamine, were also determined. The model was used to determine the protective effects of 0.5, 1 and 2 μM TQ against Meth-induced toxicity (at 1 mM). The results showed that TQ reduced Meth-induced neurotoxicity, possibly through the inhibition of ROS generation and apoptosis, and by helping to maintain GSH and dopamine levels. Thus, the impact of TQ treatment on Meth-induced neurotoxicity could warrant further investigation.
Keyphrases
- oxidative stress
- diabetic rats
- high glucose
- cell death
- growth factor
- reactive oxygen species
- flow cytometry
- dna damage
- drug induced
- stem cells
- endothelial cells
- anti inflammatory
- ischemia reperfusion injury
- high resolution
- climate change
- attention deficit hyperactivity disorder
- solid phase extraction
- endoplasmic reticulum stress
- bone marrow
- cell cycle arrest
- liquid chromatography