Repeated treatment with a low dose of reserpine as a progressive model of Parkinson's disease

Fernandes, Valéria S.; Santos, José R.; Leão, Anderson H.F.F.; Medeiros, André M.; Melo, Thieza G.; Izídio, Geison S.; Cabral, Alícia; Ribeiro, Rosana A.; Abı́lio, Vanessa C.; Ribeiro, Alessandra Mussi; Silva, Regina H.

doi:10.1016/j.bbr.2012.03.008

Cited by 100 publications

(79 citation statements)

References 79 publications

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“…As previously observed in studies by our group [8,9], repeated treatment with a low dose (0.1 mg/kg) of reserpine in rats induced the progressive appearance of motor impairment. This impairment is marked by a gradual increase in the duration of catalepsy behavior.…”

Section: Discussionsupporting

confidence: 78%

“…Second, it has been shown that reserpine treatment increases brain oxidative stress and this alteration is accompanied by behavioral deficits [10,22,23]. In addition, in a previous study [9] the repeated treatment with a low dose of reserpine induced an increase in striatal level of lipid peroxidation, which occurred concomitantly to the motor impairment. These results lead us to question if cotreatment with TOC would prevent the progressive motor and cognitive alterations induced by the repeated treatment with a low dose of reserpine.…”

Section: Discussionmentioning

confidence: 89%

“…More recently, studies have shown that the chronic administration of reserpine in low doses can promote progressive cognitive and motor impairments, along with decreased tyrosine hydroxylase levels in the nigrostriatal pathway [8]. This protocol is suggested as a progressive pharmacological model of PD [8,9].…”

Section: Introductionmentioning

confidence: 99%

“…For example, there is evidence that the inclusion of antioxidant agents in the pharmacological treatment of PD has advantages over the treatment based only in dopamine replacement [11][12][13]. In addition, the repeated treatment with reserpine that induces progressive features compatible with PD also leads to increased brain oxidative stress [9]. However, it is unclear if a possible oxidative damage is responsible for the behavioral deficits presented by animals repeatedly treated with reserpine.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Sarmento-Silva¹,

Lima²,

Cabral³

et al. 2015

Biochem Pharmacol (Los Angel)

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Sarmento-Silva¹,

Lima²,

Cabral³

et al. 2015

Biochem Pharmacol (Los Angel)

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“…14, 15 Recently, we demonstrated that reserpine treatment inhibits autophagic flux and induces autophagosome formation. 16 However, the role of reserpine in cell signaling is not fully understood.…”

mentioning

confidence: 99%

Reserpine treatment activates AMP activated protein kinase (AMPK)

et al. 2017

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− Reserpine is a well-known medicine for the treatment of hypertension, however the role of reserpine in cell signaling is not fully understood. Here, we report that reserpine treatment induces the phosphorylation of AMP activated protein kinase (AMPK) at threonine 172 (T172) in PC12 cells. Phosphorylation of AMPK T172 is regulated by upstream signaling molecules, and the increase of phospho-T172 indicates that AMPK is activated. When we examined the FOXO3a dependent transcription by using the FHRE-Luc reporter assay, reserpine treatment repressed the FHRE-Luc reporter activity in a dose dependent manner. Finally, we showed that reserpine treatment induced the phosphorylation of AMPK as well as cell death in MCF-7 cells. These results suggest that AMPK is a potential cellular target of reserpine.

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Revealing interaction between sulfobutylether‐β‐cyclodextrin and reserpine by chemiluminescence and site‐directed molecular docking

Xiong

Zhao

et al. 2013

Luminescence

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The host-guest interaction between sulfobutylether-β-cyclodextrin (SBE-β-CD) and reserpine (RSP) is described using flow injection-chemiluminescence (FI-CL) and site-directed molecular docking methods. It was found that RSP could inhibit the CL intensity produced by a luminol/SBE-β-CD system. The decrease in CL intensity was logarithmic over an RSP concentration range of 0.03 to 700.0 nM, giving a regression equation of ∆I = 107.1lgCRES + 186.1 with a detection limit of 10 pM (3σ). The CL assay was successfully applied in the determination of RSP in injection, saliva and urine samples with recoveries in the range 93.5-106.1%. Using the proposed CL model, the binding constant (KCD-R ) and the stoichiometric ratio of SBE-β-CD/RSP were calculated to be 7.4 × 10(6) M(-1) and 1 : 1, respectively. Using molecular docking, it was confirmed that luminol binds to the small cavity of SBE-β-CD with a nonpolar interaction, while RSP targeted the larger cavity of SBE-β-CD and formed a 1 : 1 complex with hydrogen bonds. The proposed new CL method has the potential to become a powerful tool for revealing the host-guest interaction between CDs and drugs, as well as monitoring drugs with high sensitivity.

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Repeated treatment with a low dose of reserpine as a progressive model of Parkinson's disease

Cited by 100 publications

References 79 publications

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Reserpine treatment activates AMP activated protein kinase (AMPK)

Revealing interaction between sulfobutylether‐β‐cyclodextrin and reserpine by chemiluminescence and site‐directed molecular docking

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