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Neuroprotective Effects of San-Huang-Xie-Xin-Tang in the MPP(+)/MPTP Models of Parkinson's Disease In Vitro and In Vivo.

Lo YC, Shih YT, Tseng YT, Hsu HT - Evid Based Complement Alternat Med (2012)

Bottom Line: SHXT reduced apoptotic signals (cytochrome and caspase) and apoptotic death.In MPTP animal model, SHXT markedly increased TH-positive neurons in the substantia nigra pars compacta (SNpc) and improved motor activity of mice.In conclusion, the present results reveal the evidence that SHXT possesses beneficial protection against MPTP-induced neurotoxicity in this model of Parkinson's disease via its antioxidative and antiapoptotic effects.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, School of Medicine, College of Medicine, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Kaohsiung 80708, Taiwan.

ABSTRACT
San-Huang-Xie-Xin-Tang (SHXT), composed of Coptidis rhizoma, Scutellariae radix, and Rhei rhizoma, is a traditional Chinese medicine used for complementary and alternative therapy of cardiovascular and neurodegenerative diseases via its anti-inflammatory and antioxidative effects. The aim of this study is to investigate the protective effects of SHXT in the 1-methyl-4-phenylpyridinium (MPP(+))/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease. Rat primary mesencephalic neurons and mouse Parkinson disease model were used in this study. Oxidative stress was induced by MPP(+) in vitro and MPTP in vivo. In MPP(+)-treated mesencephalic neuron cultures, SHXT significantly increased the numbers of TH-positive neurons. SHXT reduced apoptotic signals (cytochrome and caspase) and apoptotic death. MPP(+)-induced gp91(phox) activation and ROS production were attenuated by SHXT. In addition, SHXT increased the levels of GSH and SOD in MPP(+)-treated neurons. In MPTP animal model, SHXT markedly increased TH-positive neurons in the substantia nigra pars compacta (SNpc) and improved motor activity of mice. In conclusion, the present results reveal the evidence that SHXT possesses beneficial protection against MPTP-induced neurotoxicity in this model of Parkinson's disease via its antioxidative and antiapoptotic effects. SHXT might be a potentially alternative and complementary medicine for neuroprotection.

No MeSH data available.


Related in: MedlinePlus

Effects of SHXTon ROS level (a), gp91phox expression (b), GSH level (c), and SOD activity (d) in primary mesencephalic neurons treated with MPP+ for 48 h. Cultures were pretreated with SHXT (25–75 μg/mL) for 1 h before MPP+ treatment. ROS was determined by H2DCF-DA staining. Protein expression was detected by western blotting. GSH level and SOD activity were measured by commercial kits. Bars represent the mean ± S.E.M. from six independent experiments. Densitometry analyses are presented as the relative ratio of protein/β-actin protein and are represented as percentages of MPP+ group. #P < 0.05, ##P < 0.01 versus control (without any treatment), *P < 0.05, **P < 0.01 versus MPP+ only.
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fig3: Effects of SHXTon ROS level (a), gp91phox expression (b), GSH level (c), and SOD activity (d) in primary mesencephalic neurons treated with MPP+ for 48 h. Cultures were pretreated with SHXT (25–75 μg/mL) for 1 h before MPP+ treatment. ROS was determined by H2DCF-DA staining. Protein expression was detected by western blotting. GSH level and SOD activity were measured by commercial kits. Bars represent the mean ± S.E.M. from six independent experiments. Densitometry analyses are presented as the relative ratio of protein/β-actin protein and are represented as percentages of MPP+ group. #P < 0.05, ##P < 0.01 versus control (without any treatment), *P < 0.05, **P < 0.01 versus MPP+ only.

Mentions: As the oxidative stress is the main cause of MPP+-induced cytotoxicity, we investigated the effect of SHXT on MPP+-induced ROS generation by measuring H2DCF-DA loaded neuronal cells using flow cytometry. Results indicated MPP+-induced increase in ROS production was attenuated by SHXT pretreatment (Figure 3(a)). Moreover, MPP+-induced gp91phox overexpression, which plays an important role in ROS production, was also attenuated by SHXT pretreatment (Figure 3(b)). Furthermore, MPP+ significantly decreased GSH level and SOD activity in the rat primary neurons. However, SHXT could significantly increase GSH level (Figure 3(c)) and SOD activity (Figure 3(d)) compared with MPP+-treated group.


Neuroprotective Effects of San-Huang-Xie-Xin-Tang in the MPP(+)/MPTP Models of Parkinson's Disease In Vitro and In Vivo.

Lo YC, Shih YT, Tseng YT, Hsu HT - Evid Based Complement Alternat Med (2012)

Effects of SHXTon ROS level (a), gp91phox expression (b), GSH level (c), and SOD activity (d) in primary mesencephalic neurons treated with MPP+ for 48 h. Cultures were pretreated with SHXT (25–75 μg/mL) for 1 h before MPP+ treatment. ROS was determined by H2DCF-DA staining. Protein expression was detected by western blotting. GSH level and SOD activity were measured by commercial kits. Bars represent the mean ± S.E.M. from six independent experiments. Densitometry analyses are presented as the relative ratio of protein/β-actin protein and are represented as percentages of MPP+ group. #P < 0.05, ##P < 0.01 versus control (without any treatment), *P < 0.05, **P < 0.01 versus MPP+ only.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3303814&req=5

fig3: Effects of SHXTon ROS level (a), gp91phox expression (b), GSH level (c), and SOD activity (d) in primary mesencephalic neurons treated with MPP+ for 48 h. Cultures were pretreated with SHXT (25–75 μg/mL) for 1 h before MPP+ treatment. ROS was determined by H2DCF-DA staining. Protein expression was detected by western blotting. GSH level and SOD activity were measured by commercial kits. Bars represent the mean ± S.E.M. from six independent experiments. Densitometry analyses are presented as the relative ratio of protein/β-actin protein and are represented as percentages of MPP+ group. #P < 0.05, ##P < 0.01 versus control (without any treatment), *P < 0.05, **P < 0.01 versus MPP+ only.
Mentions: As the oxidative stress is the main cause of MPP+-induced cytotoxicity, we investigated the effect of SHXT on MPP+-induced ROS generation by measuring H2DCF-DA loaded neuronal cells using flow cytometry. Results indicated MPP+-induced increase in ROS production was attenuated by SHXT pretreatment (Figure 3(a)). Moreover, MPP+-induced gp91phox overexpression, which plays an important role in ROS production, was also attenuated by SHXT pretreatment (Figure 3(b)). Furthermore, MPP+ significantly decreased GSH level and SOD activity in the rat primary neurons. However, SHXT could significantly increase GSH level (Figure 3(c)) and SOD activity (Figure 3(d)) compared with MPP+-treated group.

Bottom Line: SHXT reduced apoptotic signals (cytochrome and caspase) and apoptotic death.In MPTP animal model, SHXT markedly increased TH-positive neurons in the substantia nigra pars compacta (SNpc) and improved motor activity of mice.In conclusion, the present results reveal the evidence that SHXT possesses beneficial protection against MPTP-induced neurotoxicity in this model of Parkinson's disease via its antioxidative and antiapoptotic effects.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, School of Medicine, College of Medicine, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Kaohsiung 80708, Taiwan.

ABSTRACT
San-Huang-Xie-Xin-Tang (SHXT), composed of Coptidis rhizoma, Scutellariae radix, and Rhei rhizoma, is a traditional Chinese medicine used for complementary and alternative therapy of cardiovascular and neurodegenerative diseases via its anti-inflammatory and antioxidative effects. The aim of this study is to investigate the protective effects of SHXT in the 1-methyl-4-phenylpyridinium (MPP(+))/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease. Rat primary mesencephalic neurons and mouse Parkinson disease model were used in this study. Oxidative stress was induced by MPP(+) in vitro and MPTP in vivo. In MPP(+)-treated mesencephalic neuron cultures, SHXT significantly increased the numbers of TH-positive neurons. SHXT reduced apoptotic signals (cytochrome and caspase) and apoptotic death. MPP(+)-induced gp91(phox) activation and ROS production were attenuated by SHXT. In addition, SHXT increased the levels of GSH and SOD in MPP(+)-treated neurons. In MPTP animal model, SHXT markedly increased TH-positive neurons in the substantia nigra pars compacta (SNpc) and improved motor activity of mice. In conclusion, the present results reveal the evidence that SHXT possesses beneficial protection against MPTP-induced neurotoxicity in this model of Parkinson's disease via its antioxidative and antiapoptotic effects. SHXT might be a potentially alternative and complementary medicine for neuroprotection.

No MeSH data available.


Related in: MedlinePlus