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Epicatechin Reduces Striatal MPP⁺-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity.

Rubio-Osornio M, Gorostieta-Salas E, Montes S, Pérez-Severiano F, Rubio C, Gómez C, Ríos C, Guevara J - Oxid Med Cell Longev (2015)

Bottom Line: Cu/Zn-dependent superoxide dismutase (Cu/Zn-SOD) activity was significantly (P < 0.05) reduced as a consequence of MPP(+) damage.Such effects persisted in animals injured with MPP(+).The results show that EC is effective against MPP(+)-induced biochemical and behavioral damage, which is possible by an increase in Cu/Zn-SOD activity.

View Article: PubMed Central - PubMed

Affiliation: Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez, 14269 Mexico City, Mexico.

ABSTRACT
Parkinson's disease is a neurodegenerative disorder characterized by movement alterations caused by reduced dopaminergic neurotransmission in the nigrostriatal pathway, presumably by oxidative stress (OS). MPP(+) intrastriatal injection leads to the overproduction of free radicals (FR). The increasing formation of FR produces OS, a decline in dopamine (DA) content, and behavioral disorders. Epicatechin (EC) has shown the ability to be FR scavenger, an antioxidant enzyme inductor, a redox state modulator, and transition metal chelator. Acute administration of 100 mg/kg of EC significantly prevented (P < 0.05) the circling MPP(+)-induced behavior (10 μg/8 μL). Likewise, EC significantly (P < 0.05) reduced the formation of fluorescent lipid products caused by MPP(+). MPP(+) injection produced (P < 0.05) increased enzymatic activity of the constitutive nitric oxide synthase (cNOS). This effect was blocked with acute EC pretreatment. Cu/Zn-dependent superoxide dismutase (Cu/Zn-SOD) activity was significantly (P < 0.05) reduced as a consequence of MPP(+) damage. EC produced a slight increase (≈20%) in Cu/Zn-SOD activity in the control group. Such effects persisted in animals injured with MPP(+). The results show that EC is effective against MPP(+)-induced biochemical and behavioral damage, which is possible by an increase in Cu/Zn-SOD activity.

No MeSH data available.


Related in: MedlinePlus

EC reduces MPP+-induced striatal lipid peroxidation in rat. Six hours after MPP+-induced damage, the formation of lipid fluorescent products was measured as an index of lipid peroxidation. The results are expressed as fluorescence arbitrary units. Each bar represents the mean ± S.E.M. of 8 animals per group. ∗P < 0.05, two-way ANOVA followed by Tukey's test.
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fig2: EC reduces MPP+-induced striatal lipid peroxidation in rat. Six hours after MPP+-induced damage, the formation of lipid fluorescent products was measured as an index of lipid peroxidation. The results are expressed as fluorescence arbitrary units. Each bar represents the mean ± S.E.M. of 8 animals per group. ∗P < 0.05, two-way ANOVA followed by Tukey's test.

Mentions: The results obtained from EC administration against MPP+-induced oxidative damage are shown in Figure 2. The formation of fluorescent lipid products was measured 6 h after MPP+ infusion as a short-term damage marker. Animals treated with the vehicle solution (oral pathway) and sterile saline (intrastriatal) were considered as the control group (1.315 ± 0.073, fluorescent units). We did not find any changes with respect to the control group with EC administration (1.347 ± 0.082) more than with the saline solution. However, MPP+ infusion statistically increased (P < 0.05) the formation of lipid fluorescent products (1.969 ± 0.179). EC pretreatment prevented the formation of oxidized lipids induced by MPP+ to levels shown in the control group (1.455 ± 0.087).


Epicatechin Reduces Striatal MPP⁺-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity.

Rubio-Osornio M, Gorostieta-Salas E, Montes S, Pérez-Severiano F, Rubio C, Gómez C, Ríos C, Guevara J - Oxid Med Cell Longev (2015)

EC reduces MPP+-induced striatal lipid peroxidation in rat. Six hours after MPP+-induced damage, the formation of lipid fluorescent products was measured as an index of lipid peroxidation. The results are expressed as fluorescence arbitrary units. Each bar represents the mean ± S.E.M. of 8 animals per group. ∗P < 0.05, two-way ANOVA followed by Tukey's test.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4537749&req=5

fig2: EC reduces MPP+-induced striatal lipid peroxidation in rat. Six hours after MPP+-induced damage, the formation of lipid fluorescent products was measured as an index of lipid peroxidation. The results are expressed as fluorescence arbitrary units. Each bar represents the mean ± S.E.M. of 8 animals per group. ∗P < 0.05, two-way ANOVA followed by Tukey's test.
Mentions: The results obtained from EC administration against MPP+-induced oxidative damage are shown in Figure 2. The formation of fluorescent lipid products was measured 6 h after MPP+ infusion as a short-term damage marker. Animals treated with the vehicle solution (oral pathway) and sterile saline (intrastriatal) were considered as the control group (1.315 ± 0.073, fluorescent units). We did not find any changes with respect to the control group with EC administration (1.347 ± 0.082) more than with the saline solution. However, MPP+ infusion statistically increased (P < 0.05) the formation of lipid fluorescent products (1.969 ± 0.179). EC pretreatment prevented the formation of oxidized lipids induced by MPP+ to levels shown in the control group (1.455 ± 0.087).

Bottom Line: Cu/Zn-dependent superoxide dismutase (Cu/Zn-SOD) activity was significantly (P < 0.05) reduced as a consequence of MPP(+) damage.Such effects persisted in animals injured with MPP(+).The results show that EC is effective against MPP(+)-induced biochemical and behavioral damage, which is possible by an increase in Cu/Zn-SOD activity.

View Article: PubMed Central - PubMed

Affiliation: Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez, 14269 Mexico City, Mexico.

ABSTRACT
Parkinson's disease is a neurodegenerative disorder characterized by movement alterations caused by reduced dopaminergic neurotransmission in the nigrostriatal pathway, presumably by oxidative stress (OS). MPP(+) intrastriatal injection leads to the overproduction of free radicals (FR). The increasing formation of FR produces OS, a decline in dopamine (DA) content, and behavioral disorders. Epicatechin (EC) has shown the ability to be FR scavenger, an antioxidant enzyme inductor, a redox state modulator, and transition metal chelator. Acute administration of 100 mg/kg of EC significantly prevented (P < 0.05) the circling MPP(+)-induced behavior (10 μg/8 μL). Likewise, EC significantly (P < 0.05) reduced the formation of fluorescent lipid products caused by MPP(+). MPP(+) injection produced (P < 0.05) increased enzymatic activity of the constitutive nitric oxide synthase (cNOS). This effect was blocked with acute EC pretreatment. Cu/Zn-dependent superoxide dismutase (Cu/Zn-SOD) activity was significantly (P < 0.05) reduced as a consequence of MPP(+) damage. EC produced a slight increase (≈20%) in Cu/Zn-SOD activity in the control group. Such effects persisted in animals injured with MPP(+). The results show that EC is effective against MPP(+)-induced biochemical and behavioral damage, which is possible by an increase in Cu/Zn-SOD activity.

No MeSH data available.


Related in: MedlinePlus