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Protection of Tong-Sai-Mai Decoction against Apoptosis Induced by H2O2 in PC12 Cells: Mechanisms via Bcl-2-Mitochondria-ROS-INOS Pathway.

Lee MK, Lu Y, Di LQ, Xu HQ - Evid Based Complement Alternat Med (2014)

Bottom Line: Meanwhile, it reduces intracellular [Ca(2+)] concentration, lactate dehydrogenase (LDH) release, and the expression of caspase-3 and bax.The results of the present study suggested that the cytoprotective effects of the TSM might be mediated, at least in part, by the bcl-2-mitochondria-ROS-INOS pathway.Due to its nontoxic characteristics, TSM could be further developed to treat the neurodegenerative diseases which are closely associated with the oxidative stress.

View Article: PubMed Central - PubMed

Affiliation: Jiangsu Engineering Research Center for Efficient Delivery System of Traditional Chinese Medicine, Nanjing 210046, China.

ABSTRACT
Tong-Sai-Mai decoction (TSM) is a Chinese materia medica polyherbal formulation that has been applied in treating brain ischemia for hundreds of years. Because it could repress the oxidative stress in in vivo studies, now we focus on the in vitro studies to investigate the mechanism by targeting the oxidative stress dependent signaling. The relation between the neurogenesis and the reactive oxygen species (ROS) production remains largely unexamined. PC12 cells are excitable cell types widely used as in vitro model for neuronal cells. Most marker genes that are related to neurotoxicity, apoptosis, and cell cycles are expressed at high levels in these cells. The aim of the present study is to explore the cytoprotection of TSM against hydrogen peroxide- (H2O2-) induced apoptosis and the molecular mechanisms underlying PC12 cells. Our findings revealed that TSM cotreatment with H2O2 restores the expression of bcl-2, inducible nitric oxide synthase (INOS), and mitochondria membrane potential. Meanwhile, it reduces intracellular [Ca(2+)] concentration, lactate dehydrogenase (LDH) release, and the expression of caspase-3 and bax. The results of the present study suggested that the cytoprotective effects of the TSM might be mediated, at least in part, by the bcl-2-mitochondria-ROS-INOS pathway. Due to its nontoxic characteristics, TSM could be further developed to treat the neurodegenerative diseases which are closely associated with the oxidative stress.

No MeSH data available.


Related in: MedlinePlus

Effect of TSM on the LDH leakage in H2O2-treated PC12 cells. The cells were treated with 200 μmol/L H2O2 and 0.05, 0.5, and 5 mg/mL TSM with 200 μmol/L H2O2. The values given are the mean ± SEM (n = 6). #P ≤ 0.05 and ##P ≤ 0.01 as compared with the control group; *P ≤ 0.05 and **P ≤ 0.01 as compared with the H2O2 group.
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fig2: Effect of TSM on the LDH leakage in H2O2-treated PC12 cells. The cells were treated with 200 μmol/L H2O2 and 0.05, 0.5, and 5 mg/mL TSM with 200 μmol/L H2O2. The values given are the mean ± SEM (n = 6). #P ≤ 0.05 and ##P ≤ 0.01 as compared with the control group; *P ≤ 0.05 and **P ≤ 0.01 as compared with the H2O2 group.

Mentions: The effect of the TSM on the LDH assay in H2O2-treated PC12 cells was shown in Figure 2. After the treatment of PC12 cells with 200 μmol/L H2O2 for 24 h, the LDH assay was significantly increased as compared with the control group. The LDH activity in H2O2 group was 49.5% while being 9.2% in control group. The cotreatment of PC12 cells with various concentrations of TSM (0.05 mg/mL, 0.5 mg/mL, and 5 mg/mL) in the presence of 200 μmol/L H2O2 for 24 h resulted in decrease of LDH activity with 38.5%, 34.33%, and 26.5%, respectively.


Protection of Tong-Sai-Mai Decoction against Apoptosis Induced by H2O2 in PC12 Cells: Mechanisms via Bcl-2-Mitochondria-ROS-INOS Pathway.

Lee MK, Lu Y, Di LQ, Xu HQ - Evid Based Complement Alternat Med (2014)

Effect of TSM on the LDH leakage in H2O2-treated PC12 cells. The cells were treated with 200 μmol/L H2O2 and 0.05, 0.5, and 5 mg/mL TSM with 200 μmol/L H2O2. The values given are the mean ± SEM (n = 6). #P ≤ 0.05 and ##P ≤ 0.01 as compared with the control group; *P ≤ 0.05 and **P ≤ 0.01 as compared with the H2O2 group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4227446&req=5

fig2: Effect of TSM on the LDH leakage in H2O2-treated PC12 cells. The cells were treated with 200 μmol/L H2O2 and 0.05, 0.5, and 5 mg/mL TSM with 200 μmol/L H2O2. The values given are the mean ± SEM (n = 6). #P ≤ 0.05 and ##P ≤ 0.01 as compared with the control group; *P ≤ 0.05 and **P ≤ 0.01 as compared with the H2O2 group.
Mentions: The effect of the TSM on the LDH assay in H2O2-treated PC12 cells was shown in Figure 2. After the treatment of PC12 cells with 200 μmol/L H2O2 for 24 h, the LDH assay was significantly increased as compared with the control group. The LDH activity in H2O2 group was 49.5% while being 9.2% in control group. The cotreatment of PC12 cells with various concentrations of TSM (0.05 mg/mL, 0.5 mg/mL, and 5 mg/mL) in the presence of 200 μmol/L H2O2 for 24 h resulted in decrease of LDH activity with 38.5%, 34.33%, and 26.5%, respectively.

Bottom Line: Meanwhile, it reduces intracellular [Ca(2+)] concentration, lactate dehydrogenase (LDH) release, and the expression of caspase-3 and bax.The results of the present study suggested that the cytoprotective effects of the TSM might be mediated, at least in part, by the bcl-2-mitochondria-ROS-INOS pathway.Due to its nontoxic characteristics, TSM could be further developed to treat the neurodegenerative diseases which are closely associated with the oxidative stress.

View Article: PubMed Central - PubMed

Affiliation: Jiangsu Engineering Research Center for Efficient Delivery System of Traditional Chinese Medicine, Nanjing 210046, China.

ABSTRACT
Tong-Sai-Mai decoction (TSM) is a Chinese materia medica polyherbal formulation that has been applied in treating brain ischemia for hundreds of years. Because it could repress the oxidative stress in in vivo studies, now we focus on the in vitro studies to investigate the mechanism by targeting the oxidative stress dependent signaling. The relation between the neurogenesis and the reactive oxygen species (ROS) production remains largely unexamined. PC12 cells are excitable cell types widely used as in vitro model for neuronal cells. Most marker genes that are related to neurotoxicity, apoptosis, and cell cycles are expressed at high levels in these cells. The aim of the present study is to explore the cytoprotection of TSM against hydrogen peroxide- (H2O2-) induced apoptosis and the molecular mechanisms underlying PC12 cells. Our findings revealed that TSM cotreatment with H2O2 restores the expression of bcl-2, inducible nitric oxide synthase (INOS), and mitochondria membrane potential. Meanwhile, it reduces intracellular [Ca(2+)] concentration, lactate dehydrogenase (LDH) release, and the expression of caspase-3 and bax. The results of the present study suggested that the cytoprotective effects of the TSM might be mediated, at least in part, by the bcl-2-mitochondria-ROS-INOS pathway. Due to its nontoxic characteristics, TSM could be further developed to treat the neurodegenerative diseases which are closely associated with the oxidative stress.

No MeSH data available.


Related in: MedlinePlus