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Neuroprotective effects of cuscutae semen in a mouse model of Parkinson's disease.

Ye M, Lee SG, Chung ES, Lim SJ, Kim WS, Yoon H, Kim SK, Ahn KS, Jang YP, Bae H - Evid Based Complement Alternat Med (2014)

Bottom Line: The MPTP-induced loss of nigral DA neurons was partly inhibited by CS-mediated decreases in ROS generation.The activation of microglia was slightly inhibited by CS, although this effect did not reach statistical significance.These results suggest that CS may be beneficial for the treatment of neurodegenerative diseases such as PD.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, College of Korean Medicine, Kyung Hee University, No. 1, Hoegi-dong, Dongdaemungu, Seoul 130-701, Republic of Korea.

ABSTRACT
Parkinson's disease (PD) is a neurodegenerative movement disorder that is characterized by the progressive degeneration of the dopaminergic (DA) pathway. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes damage to the DA neurons, and 1-4-methyl-4-phenylpyridinium (MPP(+)) causes cell death in differentiated PC12 cells that is similar to the degeneration that occurs in PD. Moreover, MPTP treatment increases the activity of the brain's immune cells, reactive oxygen species- (ROS-) generating processes, and glutathione peroxidase. We recently reported that Cuscutae Semen (CS), a widely used traditional herbal medicine, increases cell viability in a yeast model of PD. In the present study, we examined the inhibitory effect of CS on the neurotoxicity of MPTP in mice and on the MPP+-induced cell death in differentiated PC12 cells. The MPTP-induced loss of nigral DA neurons was partly inhibited by CS-mediated decreases in ROS generation. The activation of microglia was slightly inhibited by CS, although this effect did not reach statistical significance. Furthermore, CS may reduce the MPP+ toxicity in PC12 cells by suppressing glutathione peroxidase activation. These results suggest that CS may be beneficial for the treatment of neurodegenerative diseases such as PD.

No MeSH data available.


Related in: MedlinePlus

In vivo MPTP-induced DA fiber neurotoxicity in the STR. The treatment of the MPTP-injected mice with CS prevented DA neuronal death in the STR. MPTP-injected mice were treated with CS (50, 100, or 200 mg/kg) or PBS for 6 days beginning 12 h after the final MPTP injection. Seven days after the MPTP injections, brain sections were prepared and immunostained with TH antibody to identify DA fibers. The representative images were displayed (a). Scale bar was 5 mm. The densities of the TH-fibers in the STR were stereologically counted (b). The error bars represent the SEMs. **P < 0.01, ***P < 0.001, significantly different from the MPTP with PBS group. ###P < 0.001, significantly different from the saline with PBS group (one-way ANOVA and Student-Newman-Keuls analyses). The schematic brain sections are from the atlas (Paxinos and Franklin, 1997). The square represents STR in the mouse brain. C: control; M: MPTP; CS50: CS50+MPTP; CS100: CS100+MPTP; CS200: CS200+MPTP.
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fig5: In vivo MPTP-induced DA fiber neurotoxicity in the STR. The treatment of the MPTP-injected mice with CS prevented DA neuronal death in the STR. MPTP-injected mice were treated with CS (50, 100, or 200 mg/kg) or PBS for 6 days beginning 12 h after the final MPTP injection. Seven days after the MPTP injections, brain sections were prepared and immunostained with TH antibody to identify DA fibers. The representative images were displayed (a). Scale bar was 5 mm. The densities of the TH-fibers in the STR were stereologically counted (b). The error bars represent the SEMs. **P < 0.01, ***P < 0.001, significantly different from the MPTP with PBS group. ###P < 0.001, significantly different from the saline with PBS group (one-way ANOVA and Student-Newman-Keuls analyses). The schematic brain sections are from the atlas (Paxinos and Franklin, 1997). The square represents STR in the mouse brain. C: control; M: MPTP; CS50: CS50+MPTP; CS100: CS100+MPTP; CS200: CS200+MPTP.

Mentions: In the brain, MPTP is metabolized to 1-methyl-4-phenylpyridinium (MPP+), which is the active toxic compound that is primarily responsible for the neurotoxicity of MPTP [4]. MPTP was rapidly eliminated and nearly undetectable at 6 h, and striatal MPP+ levels peaked within 30 min and subsequently declined steadily until they were no longer significantly different from the controls after 12 h [5]. Accordingly, CS was administered 12 h after the final injection of MPTP in all in vivo experiments to avoid interfering with the metabolism of MPTP. To examine the neuroprotective effect of CS, MPTP-injected mice were treated with CS (50, 100, or 200 mg/kg) or PBS for 6 days. Seven days after the MPTP injection, brain sections were immunostained with an anti-TH antibody to detect DA neurons (Figure 5(a)). In the MPTP-injected mice, there was a significant reduction in the density of TH+ fibers in the STR (55%; P < 0.001; Figure 5(b)) compared to the PBS-injected control mice. CS treatment effectively blocked the reduction in the density of TH+ fibers in the STR by 23% (P < 0.001; Figure 5(b)) compared to the MPTP mice.


Neuroprotective effects of cuscutae semen in a mouse model of Parkinson's disease.

Ye M, Lee SG, Chung ES, Lim SJ, Kim WS, Yoon H, Kim SK, Ahn KS, Jang YP, Bae H - Evid Based Complement Alternat Med (2014)

In vivo MPTP-induced DA fiber neurotoxicity in the STR. The treatment of the MPTP-injected mice with CS prevented DA neuronal death in the STR. MPTP-injected mice were treated with CS (50, 100, or 200 mg/kg) or PBS for 6 days beginning 12 h after the final MPTP injection. Seven days after the MPTP injections, brain sections were prepared and immunostained with TH antibody to identify DA fibers. The representative images were displayed (a). Scale bar was 5 mm. The densities of the TH-fibers in the STR were stereologically counted (b). The error bars represent the SEMs. **P < 0.01, ***P < 0.001, significantly different from the MPTP with PBS group. ###P < 0.001, significantly different from the saline with PBS group (one-way ANOVA and Student-Newman-Keuls analyses). The schematic brain sections are from the atlas (Paxinos and Franklin, 1997). The square represents STR in the mouse brain. C: control; M: MPTP; CS50: CS50+MPTP; CS100: CS100+MPTP; CS200: CS200+MPTP.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig5: In vivo MPTP-induced DA fiber neurotoxicity in the STR. The treatment of the MPTP-injected mice with CS prevented DA neuronal death in the STR. MPTP-injected mice were treated with CS (50, 100, or 200 mg/kg) or PBS for 6 days beginning 12 h after the final MPTP injection. Seven days after the MPTP injections, brain sections were prepared and immunostained with TH antibody to identify DA fibers. The representative images were displayed (a). Scale bar was 5 mm. The densities of the TH-fibers in the STR were stereologically counted (b). The error bars represent the SEMs. **P < 0.01, ***P < 0.001, significantly different from the MPTP with PBS group. ###P < 0.001, significantly different from the saline with PBS group (one-way ANOVA and Student-Newman-Keuls analyses). The schematic brain sections are from the atlas (Paxinos and Franklin, 1997). The square represents STR in the mouse brain. C: control; M: MPTP; CS50: CS50+MPTP; CS100: CS100+MPTP; CS200: CS200+MPTP.
Mentions: In the brain, MPTP is metabolized to 1-methyl-4-phenylpyridinium (MPP+), which is the active toxic compound that is primarily responsible for the neurotoxicity of MPTP [4]. MPTP was rapidly eliminated and nearly undetectable at 6 h, and striatal MPP+ levels peaked within 30 min and subsequently declined steadily until they were no longer significantly different from the controls after 12 h [5]. Accordingly, CS was administered 12 h after the final injection of MPTP in all in vivo experiments to avoid interfering with the metabolism of MPTP. To examine the neuroprotective effect of CS, MPTP-injected mice were treated with CS (50, 100, or 200 mg/kg) or PBS for 6 days. Seven days after the MPTP injection, brain sections were immunostained with an anti-TH antibody to detect DA neurons (Figure 5(a)). In the MPTP-injected mice, there was a significant reduction in the density of TH+ fibers in the STR (55%; P < 0.001; Figure 5(b)) compared to the PBS-injected control mice. CS treatment effectively blocked the reduction in the density of TH+ fibers in the STR by 23% (P < 0.001; Figure 5(b)) compared to the MPTP mice.

Bottom Line: The MPTP-induced loss of nigral DA neurons was partly inhibited by CS-mediated decreases in ROS generation.The activation of microglia was slightly inhibited by CS, although this effect did not reach statistical significance.These results suggest that CS may be beneficial for the treatment of neurodegenerative diseases such as PD.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, College of Korean Medicine, Kyung Hee University, No. 1, Hoegi-dong, Dongdaemungu, Seoul 130-701, Republic of Korea.

ABSTRACT
Parkinson's disease (PD) is a neurodegenerative movement disorder that is characterized by the progressive degeneration of the dopaminergic (DA) pathway. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes damage to the DA neurons, and 1-4-methyl-4-phenylpyridinium (MPP(+)) causes cell death in differentiated PC12 cells that is similar to the degeneration that occurs in PD. Moreover, MPTP treatment increases the activity of the brain's immune cells, reactive oxygen species- (ROS-) generating processes, and glutathione peroxidase. We recently reported that Cuscutae Semen (CS), a widely used traditional herbal medicine, increases cell viability in a yeast model of PD. In the present study, we examined the inhibitory effect of CS on the neurotoxicity of MPTP in mice and on the MPP+-induced cell death in differentiated PC12 cells. The MPTP-induced loss of nigral DA neurons was partly inhibited by CS-mediated decreases in ROS generation. The activation of microglia was slightly inhibited by CS, although this effect did not reach statistical significance. Furthermore, CS may reduce the MPP+ toxicity in PC12 cells by suppressing glutathione peroxidase activation. These results suggest that CS may be beneficial for the treatment of neurodegenerative diseases such as PD.

No MeSH data available.


Related in: MedlinePlus