Oxidopamine hydrobromide (6-OHDA hydrobromide), an antagonist of the neurotransmitter dopamine, is a widely used neurotoxin that selectively destroys dopaminergic neurons. 6-OHDA-induced apoptosis of PC12 cells was initiated by superoxide generation followed by caspase cascade activation, which was associated with the suppressed Akt phosphorylation and increased p38 phosphorylation[3]. Moreover, the reduction in proteasomal activity by 6-OHDA was attenuated in SH-SY5Y cells pretreated with 1 μM CA(carnosic acid) [4]. Buspirone improves the anti-cataleptic effect of L-DOPA in a 6-OHDA-induced animal model of PD through the activation of 5-HT(1A) receptors[5].
Oxidopamine hydrobromide/6-羟基多巴胺氢溴酸盐 细胞实验
Cell Line
Concentration
Treated Time
Description
References
BV2 cells
60 µM
1 hour
6-OHDA-dependent ROS production in BV2 cells was markedly suppressed by Alb–Trx
Int J Mol Sci. 2023 Jun 5;24(11):9758
GT1-7 cells
10–60 µM
1 hour
6-OHDA promoted ROS production in a concentration-dependent manner, Alb–Trx significantly inhibited this effect
Int J Mol Sci. 2023 Jun 5;24(11):9758
SH-SY5Y cells
100 µM
12 or 18 hours
To evaluate the neurotoxicity of 6-OHDA on SH-SY5Y cells, including apoptosis, decreased mitochondrial membrane potential, DNA fragmentation, and increased ROS production. SRG pretreatment reversed these effects.
Cells. 2023 Sep 19;12(18):2310.
Rat primary cortical neurons
50 µM
16 hours
To evaluate the effect of 6-OHDA on neuronal survival, results showed that 6-OHDA exposure induced a reduction in cell viability.
6-OHDA induced ISR-related gene expression, Alb–Trx pretreatment suppressed these changes
Int J Mol Sci. 2023 Jun 5;24(11):9758
SH-SY5Y cells
200 µM
2 hours
To evaluate the oxidative damage and neurotoxicity of 6-OHDA on SH-SY5Y cells, the results showed that 6-OHDA induced apoptosis, ROS and O2•− formation, and loss of mitochondrial membrane potential.
Int J Mol Sci. 2012;13(9):10899-10910
SH-SY5Y cells
300 µM
2 hours
To investigate the effect of 6-OHDA on SH-SY5Y cell viability, it was found that treatment with 300 μM 6-OHDA for 2 hours significantly reduced cell viability, with a lethality rate reaching 50%.
Nutrients. 2022 Apr 4;14(7):1504
GT1-7 cells
40 µM
2 hours
6-OHDA upregulated phosphorylated JNK and downregulated phosphorylated ERK, Alb–Trx pretreatment significantly suppressed these changes
Int J Mol Sci. 2023 Jun 5;24(11):9758
B65 cells
500 µM
20 hours
To study the toxicity of 6-OHDA on B65 cells and the protective effects of antioxidants. Results showed that 6-OHDA caused cell injury, and antioxidants such as catalase and metalloporphyrin antioxidants provided protection within a certain time frame.
Free Radic Biol Med. 2007 Aug 1;43(3):372-83
PC-12 cells
40 µM
24 hours
To investigate the effect of 6-OHDA on PC-12 cell viability, results showed that 6-OHDA significantly reduced cell viability.
Neurotherapeutics. 2020 Oct;17(4):1796-1812
GT1-7 cells
40 µM
24 hours
Alb–Trx pretreatment significantly suppressed 6-OHDA-dependent decrease in cell viability
Evaluated 6-OHDA-induced toxicity and the protective effect of miR-124-3p sEVs, showing that 3×10^9 particles/mL miR-124-3p sEVs significantly protected cells from 6-OHDA toxicity.
Mol Ther. 2022 Oct 5;30(10):3176-3192
SH-SY5Y cells
6.25, 12.5, 25, 50 µM
24 hours
Evaluation of 6-OHDA neurotoxicity on SH-SY5Y cells, showing dose- and time-dependent toxicity.
Int J Mol Sci. 2022 Mar 10;23(6):3009
Human dopaminergic neuroblastoma SH-SY5Y cells
200 µM
24 hours
To evaluate 6-OHDA-induced cytotoxicity and the protective effect of hyperoside, results showed hyperoside significantly inhibited 6-OHDA-induced loss of cell viability and LDH release.
Int J Mol Sci. 2019 Nov 20;20(23):5832
SH-SY5Y neuroblastoma cells
60 µM
24 hours
Investigation of the neurotoxic effects of 6-OHDA on SH-SY5Y cells, including oxidative stress, mitochondrial damage, and apoptosis. Results showed that 6-OHDA induced caspase-3/PARP1 cleavage, DNA fragmentation, phosphatidylserine externalization, mitochondrial depolarization, and damage.
Int J Mol Sci. 2024 Oct 3;25(19):10659
BV2 microglial cells
10 µM
24 hours
6-OHDA specifically upregulated the expression of DMT1 but did not affect the expression of FPN1, which might be associated with the upregulation of IRP1.
Biomolecules. 2022 Feb 7;12(2):266
GT1-7 cells
40 µM
24 hours
Alb–Trx significantly inhibited 6-OHDA-induced neuronal cell death
Evaluate the protective effect of ergothioneine on 6-OHDA-induced cell death, showing significant improvement in cell viability
Cells. 2024 Jan 25;13(3):230
GT1-7 cells
20-80 µM
24 hours
Evaluate the effect of 6-OHDA on GT1-7 cell viability, showing a concentration-dependent decrease in cell viability
Cells. 2024 Jan 25;13(3):230
SN4741 cells
10 µM
4 hours
To investigate the cytotoxic effects of 6-OHDA on SN4741 cells, results showed that 6-OHDA significantly increased the levels of ER stress markers BiP, p-PERK, and p-IRE1.
Neurosci Bull. 2016 Feb;32(1):61-9
GT1-7 cells
40 µM
6 hours
6-OHDA reduced IκBα expression, Alb–Trx pretreatment significantly suppressed this downregulation
Int J Mol Sci. 2023 Jun 5;24(11):9758
GT1-7 cells
10–40 µM
6 hours
6-OHDA induced pro-inflammatory cytokine expression, Alb–Trx pretreatment almost fully blocked these changes
Int J Mol Sci. 2023 Jun 5;24(11):9758
Oxidopamine hydrobromide/6-羟基多巴胺氢溴酸盐 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
Partial Parkinsonism lesion model
Medial forebrain bundle injection
0.7 μg or 1.5 μg
Single injection, duration of 6 weeks
Analyzed the survival of different mDA neuron groups after 6-OHDA lesions, finding that Sox6 territory neurons were more vulnerable, while Ebf1 territory neurons were more resilient.
Elife. 2024 Apr 8;12:RP89482
Wistar male rats
6-OHDA-induced Parkinson’s disease rat model
Intrastriatal injection
10 µg
Single injection
To investigate the role of 6-OHDA in inducing neurobehavioral deficits and oxidative stress response in Parkinson’s disease rat models. Results showed that 6-OHDA induction led to neurobehavioral deficits and increased oxidative stress, which could be alleviated by FMT or NMNAT2 overexpression.
J Neuroinflammation. 2023 May 19;20(1):117
Rats
Parkinson's disease model
Intrastriatal injection
12 μg per striatum
Single injection, evaluated after 40 days
To study the impact of 6-OHDA-induced Parkinson's disease model on cardiac metabolism, showing significant changes in cardiac metabolites.
Int J Mol Sci. 2023 Jul 30;24(15):12202
Wistar rats
Parkinson's disease model
Intra-MFB injection
20μg
Single injection
Induce Parkinson's disease model and evaluate the therapeutic effects of EVs
Stem Cells Transl Med. 2019 May;8(5):490-499
Rats
6-hydroxydopamine-induced hemi-parkinsonian model
Unilateral injection into the medial forebrain bundle
26 mg
Single injection, recovery for 2-3 weeks
To assess the effect of 6-OHDA-induced dopaminergic neuronal loss on glutamate release in the GP and STN during STN-DBS. Results showed that 6-OHDA treatment altered glutamate dynamics in the GP but not in the STN.
Biosensors (Basel). 2023 Apr 16;13(4):480
Mice
6-hydroxydopamine mouse model of Parkinson’s disease
Stereotactic injection
3 μg
Single injection, recovery for 3 weeks
To investigate whether repressing PTBP1 could convert reactive astrocytes to dopaminergic neurons in a PD model. Results showed that repressing PTBP1 failed to convert astrocytes to dopaminergic neurons.
Elife. 2022 May 10;11:e75636
Sprague-Dawley rats
6-hydroxydopamine (6-OHDA) lesion model
Stereotaxic injection into the medial forebrain bundle
3.5 μg/μl
Single injection
To study the effects of 6-OHDA lesion on motor behavior and dopaminergic neurons in the brain
Br J Pharmacol. 2021 Jun;178(12):2516-2532
Male C57BL/6J mice
Parkinson's disease model
Bilateral dorsal striatum local injection
4 µg
Single injection, 3 weeks recovery
Evaluated apathy-like behavior in a Parkinson's disease model, showing significant reductions in novelty-seeking behavior in the 6-OHDA group in the hole-board test and three-chamber test.
Int J Mol Sci. 2024 Jul 22;25(14):7993
Caenorhabditis elegans
BZ555 (expressing GFP-labeled DA neurons), NL5901 (expressing YFP-fused human α-synuclein), and DA2123 (expressing GFP-fused LGG-1 protein) strains
Soaking
50 mM
Single treatment, lasting 1 hour
To evaluate the effects of 6-OHDA on DA neuron degeneration, food-sensitive behavior, lifespan, and α-synuclein accumulation in C. elegans. SRG pretreatment ameliorated these effects.
Cells. 2023 Sep 19;12(18):2310.
Sprague-Dawley rats
6-hydroxydopamine (6-OHDA)-lesioned or 6-OHDA-lesioned and L-DOPA-treated (6-OHDA/ L-DOPA) rats
Injection into the right medial forebrain bundle
7.5 and 6 μl (3.5 μg/μl)
Single injection
To investigate the effect of 6-OHDA lesion and L-DOPA treatment on the effect of buspirone in the SNr. Results showed that local buspirone inhibited SNr neuron activity in all groups, while systemic buspirone reduced burst activity in 6-OHDA-lesioned rats.
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