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Oral treatment with the herbal formula B401 protects against aging-dependent neurodegeneration by attenuating oxidative stress and apoptosis in the brain of R6/2 mice.

Wang SE, Lin CL, Hsu CH, Sheu SJ, Wu CH - Clin Interv Aging (2015)

Bottom Line: R6/2 HD mice with oral B401 treatment significantly reduced reactive oxygen species levels in the blood, but markedly increased expressions of superoxide dismutase 2 in the brain tissue.Furthermore, R6/2 HD mice with oral B401 treatment significantly increased expressions of B-cell lymphoma 2 (Bcl-2), but significantly reduced expressions of Bcl-2-associated X protein (Bax), calpain, and caspase-3 in the brain tissue.We suggest that the herbal formula B401 can be developed as a potential health supplement for ameliorating aging-dependent neurodegeneration.

View Article: PubMed Central - PubMed

Affiliation: Department of Life Science, National Taiwan Normal University, Taipei, Taiwan ; Department of Pathological Inspection, Saint Paul's Hospital, Taoyuan, Taiwan.

ABSTRACT

Background: Neurodegeneration is characterized by progressive neurological deficits due to selective neuronal loss in the nervous system. Huntington's disease (HD) is an incurable neurodegenerative disorder. Neurodegeneration in HD patients shows aging-dependent pattern. Our previous study has suggested that a herbal formula B401 may have neuroprotective effects in the brains of R6/2 mice.

Objective: To clarify possible mechanisms for neurodegeneration, which improves the understanding the aging process. This study focuses on clarifying neurodegenerative mechanisms and searching potential therapeutic targets in HD patients.

Methods: The oxidative stress and apoptosis were compared in the brain tissue between R6/2 HD mice with and without oral B401 treatment. Expressions of proteins for oxidative stress and apoptosis in the brain tissue of R6/2 HD mice were examined by using immunostaining and Western blotting techniques.

Results: R6/2 HD mice with oral B401 treatment significantly reduced reactive oxygen species levels in the blood, but markedly increased expressions of superoxide dismutase 2 in the brain tissue. Furthermore, R6/2 HD mice with oral B401 treatment significantly increased expressions of B-cell lymphoma 2 (Bcl-2), but significantly reduced expressions of Bcl-2-associated X protein (Bax), calpain, and caspase-3 in the brain tissue.

Conclusion: Our findings provide evidence that the herbal formula B401 can remedy for aging-dependent neurodegeneration of R6/2 mice via suppressing oxidative stress and apoptosis in the brain. We suggest that the herbal formula B401 can be developed as a potential health supplement for ameliorating aging-dependent neurodegeneration.

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Related in: MedlinePlus

ROS levels in the blood of the R6/2 (HD) mice were reduced under oral B401 treatment.Notes: (A) Chemiluminescence analysis shows that the expressions of ROS in the blood of the 10-week-old R6/2 mice given the oral B401 treatment were obviously weaker than those given the sham treatment but were obviously more intense than their WT. (B) The quantified expression blood levels of ROS in the 10-week-old R6/2 mice given the oral B401 treatment were significantly lower than those mice given the sham treatment. The number of R6/2 mice under oral B401 and sham treatments was six for each group. Values are mean ± SEM (**P<0.01, one-way ANOVA followed by a Student–Newman–Keuls multiple comparison posttest).Abbreviations: ECL, electro-chemiluminescence; HD, Huntington’s disease; ROS, reactive oxygen species; WT, wild-type littermate; ANOVA, analysis of variance; SEM, standard error of the mean.
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f5-cia-10-1825: ROS levels in the blood of the R6/2 (HD) mice were reduced under oral B401 treatment.Notes: (A) Chemiluminescence analysis shows that the expressions of ROS in the blood of the 10-week-old R6/2 mice given the oral B401 treatment were obviously weaker than those given the sham treatment but were obviously more intense than their WT. (B) The quantified expression blood levels of ROS in the 10-week-old R6/2 mice given the oral B401 treatment were significantly lower than those mice given the sham treatment. The number of R6/2 mice under oral B401 and sham treatments was six for each group. Values are mean ± SEM (**P<0.01, one-way ANOVA followed by a Student–Newman–Keuls multiple comparison posttest).Abbreviations: ECL, electro-chemiluminescence; HD, Huntington’s disease; ROS, reactive oxygen species; WT, wild-type littermate; ANOVA, analysis of variance; SEM, standard error of the mean.

Mentions: In comparing the effect of B401 treatment on oxidative stress, we examined the blood levels of ROS in 10-week-old R6/2 mice given the oral B401 and sham treatments by using a CLA-ID3 chemiluminescence analyzer. We observed that blood levels of ROS in the 10-week-old R6/2 mice given the sham treatment greatly increased beyond those of R6/2 mice given the oral B401 treatment (Figure 5A). Furthermore, total counts of blood ROS in the 10-week-old R6/2 mice given the sham treatment significantly increased beyond those of the R6/2 mice given the oral B401 treatment (Figure 5B, P<0.01). In this study, we also compared SOD2 in the brains of the 10-week-old R6/2 mice given the oral B401 and sham treatments, and their WT by IHC staining and Western blotting analysis in Figure 6. SOD2 is an important antioxidant enzyme for oxidative stress.15 As observed from IHC staining of the brain, expressions of SOD2 were not obvious in the striatum, hippocampus, and medulla of R6/2 mice given the sham treatment, but were obvious in the stratum, hippocampus, and medulla of R6/2 mice given the oral B401 treatment, and their WT (Figure 6A). As analyzed from Western blotting analysis of the brain, quantified SOD2 levels in the 10-week-old R6/2 mice given the sham treatment were significantly reduced when compared with those of the 10-week-old R6/2 mice given the oral B401 treatment, and their WT (Figure 6Bi and Bii, P<0.01). SOD2 levels of the 10-week-old R6/2 mice given the oral B401 treatment were not significant in comparison with those of their WT (Figure 6Bi and Bii, P>0.05).


Oral treatment with the herbal formula B401 protects against aging-dependent neurodegeneration by attenuating oxidative stress and apoptosis in the brain of R6/2 mice.

Wang SE, Lin CL, Hsu CH, Sheu SJ, Wu CH - Clin Interv Aging (2015)

ROS levels in the blood of the R6/2 (HD) mice were reduced under oral B401 treatment.Notes: (A) Chemiluminescence analysis shows that the expressions of ROS in the blood of the 10-week-old R6/2 mice given the oral B401 treatment were obviously weaker than those given the sham treatment but were obviously more intense than their WT. (B) The quantified expression blood levels of ROS in the 10-week-old R6/2 mice given the oral B401 treatment were significantly lower than those mice given the sham treatment. The number of R6/2 mice under oral B401 and sham treatments was six for each group. Values are mean ± SEM (**P<0.01, one-way ANOVA followed by a Student–Newman–Keuls multiple comparison posttest).Abbreviations: ECL, electro-chemiluminescence; HD, Huntington’s disease; ROS, reactive oxygen species; WT, wild-type littermate; ANOVA, analysis of variance; SEM, standard error of the mean.
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Related In: Results  -  Collection

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f5-cia-10-1825: ROS levels in the blood of the R6/2 (HD) mice were reduced under oral B401 treatment.Notes: (A) Chemiluminescence analysis shows that the expressions of ROS in the blood of the 10-week-old R6/2 mice given the oral B401 treatment were obviously weaker than those given the sham treatment but were obviously more intense than their WT. (B) The quantified expression blood levels of ROS in the 10-week-old R6/2 mice given the oral B401 treatment were significantly lower than those mice given the sham treatment. The number of R6/2 mice under oral B401 and sham treatments was six for each group. Values are mean ± SEM (**P<0.01, one-way ANOVA followed by a Student–Newman–Keuls multiple comparison posttest).Abbreviations: ECL, electro-chemiluminescence; HD, Huntington’s disease; ROS, reactive oxygen species; WT, wild-type littermate; ANOVA, analysis of variance; SEM, standard error of the mean.
Mentions: In comparing the effect of B401 treatment on oxidative stress, we examined the blood levels of ROS in 10-week-old R6/2 mice given the oral B401 and sham treatments by using a CLA-ID3 chemiluminescence analyzer. We observed that blood levels of ROS in the 10-week-old R6/2 mice given the sham treatment greatly increased beyond those of R6/2 mice given the oral B401 treatment (Figure 5A). Furthermore, total counts of blood ROS in the 10-week-old R6/2 mice given the sham treatment significantly increased beyond those of the R6/2 mice given the oral B401 treatment (Figure 5B, P<0.01). In this study, we also compared SOD2 in the brains of the 10-week-old R6/2 mice given the oral B401 and sham treatments, and their WT by IHC staining and Western blotting analysis in Figure 6. SOD2 is an important antioxidant enzyme for oxidative stress.15 As observed from IHC staining of the brain, expressions of SOD2 were not obvious in the striatum, hippocampus, and medulla of R6/2 mice given the sham treatment, but were obvious in the stratum, hippocampus, and medulla of R6/2 mice given the oral B401 treatment, and their WT (Figure 6A). As analyzed from Western blotting analysis of the brain, quantified SOD2 levels in the 10-week-old R6/2 mice given the sham treatment were significantly reduced when compared with those of the 10-week-old R6/2 mice given the oral B401 treatment, and their WT (Figure 6Bi and Bii, P<0.01). SOD2 levels of the 10-week-old R6/2 mice given the oral B401 treatment were not significant in comparison with those of their WT (Figure 6Bi and Bii, P>0.05).

Bottom Line: R6/2 HD mice with oral B401 treatment significantly reduced reactive oxygen species levels in the blood, but markedly increased expressions of superoxide dismutase 2 in the brain tissue.Furthermore, R6/2 HD mice with oral B401 treatment significantly increased expressions of B-cell lymphoma 2 (Bcl-2), but significantly reduced expressions of Bcl-2-associated X protein (Bax), calpain, and caspase-3 in the brain tissue.We suggest that the herbal formula B401 can be developed as a potential health supplement for ameliorating aging-dependent neurodegeneration.

View Article: PubMed Central - PubMed

Affiliation: Department of Life Science, National Taiwan Normal University, Taipei, Taiwan ; Department of Pathological Inspection, Saint Paul's Hospital, Taoyuan, Taiwan.

ABSTRACT

Background: Neurodegeneration is characterized by progressive neurological deficits due to selective neuronal loss in the nervous system. Huntington's disease (HD) is an incurable neurodegenerative disorder. Neurodegeneration in HD patients shows aging-dependent pattern. Our previous study has suggested that a herbal formula B401 may have neuroprotective effects in the brains of R6/2 mice.

Objective: To clarify possible mechanisms for neurodegeneration, which improves the understanding the aging process. This study focuses on clarifying neurodegenerative mechanisms and searching potential therapeutic targets in HD patients.

Methods: The oxidative stress and apoptosis were compared in the brain tissue between R6/2 HD mice with and without oral B401 treatment. Expressions of proteins for oxidative stress and apoptosis in the brain tissue of R6/2 HD mice were examined by using immunostaining and Western blotting techniques.

Results: R6/2 HD mice with oral B401 treatment significantly reduced reactive oxygen species levels in the blood, but markedly increased expressions of superoxide dismutase 2 in the brain tissue. Furthermore, R6/2 HD mice with oral B401 treatment significantly increased expressions of B-cell lymphoma 2 (Bcl-2), but significantly reduced expressions of Bcl-2-associated X protein (Bax), calpain, and caspase-3 in the brain tissue.

Conclusion: Our findings provide evidence that the herbal formula B401 can remedy for aging-dependent neurodegeneration of R6/2 mice via suppressing oxidative stress and apoptosis in the brain. We suggest that the herbal formula B401 can be developed as a potential health supplement for ameliorating aging-dependent neurodegeneration.

Show MeSH
Related in: MedlinePlus