| 包装: | 50mg |
| 市场价: | 360元 |
Cell lines | Primary nigral cells (PNCs) |
Preparation Method | The conditioned media were replaced with new media containing AS-IV at the final concentration indicated with or without 200 µM of 6-Hydroxydopamine hydrobromide. |
Reaction Conditions | 200µM for 24 hours |
Applications | Compared with vehicle controls, exposure to 200 µM 6-Hydroxydopamine resulted in the loss of 75% of PNCs, as determined using the LDH assay. |
Animal models | Female Sprague-Dawley rats |
Preparation Method | The animals received a single, intrastriatal injection of 6-Hydroxydopamine hydrobromide. Twenty-five micrograms of 6-Hydroxydopamine hydrobromide, which was dissolved in 1.5 µl of normal saline with 0.2% ascorbic acid, was injected at a depth of 5.6 mm ventral to the skull at the same anterior/posterior and medial/lateral coordinates at which the cells had been injected. The injection site was chosen to be midway between the two implant sites. 6-Hydroxydopamine hydrobromide was injected over 5 min, and the needle was left in place for an additional 5 min before withdrawal of the needle. |
Dosage form | 25 µg in 1.5 µl of normal saline with 0.2% ascorbic acid |
Applications | Induced neurodegeneration in the SNc by unilateral injection of 6-hydroxydopamine hydrobromide into mfb, act as 6-OHDA lesion model |
| 产品描述 | 6-Hydroxydopamine hydrobromide (6-OHDA) is a structural analogue of catecholamines, dopamine and noradrenaline, and exerts its toxic effects on catecholaminergic neurons. The neurotoxin 6-hydroxydopamine continues to constitute a valuable topical tool used chiefly in modeling Parkinson's disease (PD) in the rat[1]. The classical method of intracerebral infusion of 6-Hydroxydopamine hydrobromide, involving a massive destruction of nigrostriatal dopaminergic neurons, is largely used to investigate motor and biochemical dysfunctions in Parkinson's disease[1] 6-Hydroxydopamine hydrobromide undergoes robust auto-oxidation generating cytotoxic H2O2, reactive oxygen species (ROS) and catecholamine quinones which attack endocellular nucleophilic groups[2]. Neurotoxic effects of 6-Hydroxydopamine hydrobromide occur through a two-step mechanism involving accumulation of the toxin into catecholaminergic neurons, followed by alteration of cellular homeostasis and neuronal damage. Intracellular storage of 6-Hydroxydopamine hydrobromide is mediated by the dopamine or noradrenaline membrane transporters (DAT and NAT respectively), which recognize and uptake 6-Hydroxydopamine hydrobromide due to its structural similarity with endogenous catecholamines[3]. 6-Hydroxydopamine hydrobromide is infused unilaterally in the MFB, producing a functional imbalance between the dopaminergic nigrostriatal systems and resulting in motor slowness, indicative of parkinsonian-like akinesia, and typical rotational behaviour in response to dopaminomimetic agents[4]. References: |
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