Reserpine (hydrochloride)
CAS No. : 16994-56-2
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| Cat. No. : | HY-N0480A |
| M.Wt: | 645.14 |
| Formula: | C33H41ClN2O9 |
| Purity: | >98 % |
| Solubility: | H2O : < 0.1 mg/mL (ultrasonic;warming;heat to 80°C);DMSO : 50 mg/mL (ultrasonic) |
Reserpine hydrochloride is an inhibitor of the vesicular monoamine transporter 2 (VMAT2).
IC50 & Target:VMAT2[1]
In Vitro:Reserpine hydrochloride is an inhibitor of the vesicular monoamine transporter 2 (VMAT2). Reserpine hydrochloride displays a significant on the density of dopamine D1 receptors (F2,12=8.81, p<0.01) in the rat striatum. The affinity (Kd) for the dopamine D1 and D2 receptors during withdrawal from acute and chronic administration of reserpine is not change[1]. IC50 values of 43.9 and 54.9 μM are obtained after 1 day of treatment with Reserpine hydrochloride in JB6 P+ and HepG2-C8 cells, respectively. Reserpine hydrochloride induces luciferase activity in a dose-dependent manner at concentrations ranging from 5 to 50 μM, and no significant induction is observed at concentrations lower than 5 μM. Results demonstrate that Reserpine hydrochloride (2.5 to 10 μM) also increases the protein expression of Nrf2, HO-1, and NQO1. Reserpine hydrochloride at concentrations of 2.5 to 10 μM decreases the mRNA expression of DNMT1, DNMT3a, and DNMT3b in a concentration-dependent manner in JB6 P+ cells after 7 days of treatment. Reserpine hydrochloride at 10 μM generates a significant difference for DNMT3a expression (p<0.05)[2].
In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.
Reserpine can be used in animal modeling to create gastrointestinal ulcer and depression models. Withdrawal from chronic (14 days) but not acute reserpine (48 hours) significantly decreases immobility time (F2,18=3.68, p<0.05) and increases climbing time (F2,18=4.48, p<0.02) in rats, without altering swimming time in the forced swim test (FST) (F2,18=1.78; NS) compared to control animals. A dose of 5 mg/kg body weight of Reserpine significantly increases the urinary excretion of vanillylmandelic acid (VMA). Animals treated with Reserpine excrete more 5-hydroxyindoleacetic acid (5-HIAA) than controls. Reserpine treatment results in dose-dependent hypotension. Compared to controls, doses of 0.5, 1, 5, 10, and 15 μg/kg of Reserpine significantly (p<0.01) reduce blood pressure[1][3].
Administration: 5 mg/kg • ip • 18 h before sacrifice
Mice: ICR mice • male • 7 weeks old[5]
Administration: 10 mg/kg • ip • once daily for 3 days
(2)The level of cancer induction was identified by specific biochemical markers such as serum gastrin level, TBARS, and glutathione followed by histopathological analysis at two-time periods for 8 and 16 week.
Molecular changes: In the reserpine-induced gastric ulcer control mice, the gastric secretion volume was increased, the pH value (1.04) was decreased, the serum cytokine levels of IL-6, IL-12, TNF-α and IFN-γ was increased.
Administration: 0.5 mg/kg • ip • once per day for 14 days
Mice: C57BL/6 mice • male • 7 weeks old[8]
Administration: 0.5 mg/kg • ip • once per day for 10 days
Molecular changes: Reserpine administration significantly increased cortical contents of MDA (malondialdehyde), reduced GSH (glutathione), increased TNF-ɑ and reduced BDNF (brain derived neurotropic factor). Showed a significant decrease in cortical nor-epinephrine (NE), serotonin (5-HT), and dopamine (DA)
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