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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

The cell cycle modifications induced by TSM. (a) Control group. The cells were treated with 200 μmol/L H2O2 (b) and 0.05, 0.5, and 5 mg/mL TSM in the presence of 200 μmol/L H2O2 ((c), (d), and (e)). The blue color represented the diploid G1 phase; the red color represented the diploid G2 phase; and the grey color represented the diploid S phase. The percentage of G1, G2, and S in cells treated with 200 μmol/L H2O2 and various concentrations of TSM and cumulative data from three independent experiments were shown.
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fig7: The cell cycle modifications induced by TSM. (a) Control group. The cells were treated with 200 μmol/L H2O2 (b) and 0.05, 0.5, and 5 mg/mL TSM in the presence of 200 μmol/L H2O2 ((c), (d), and (e)). The blue color represented the diploid G1 phase; the red color represented the diploid G2 phase; and the grey color represented the diploid S phase. The percentage of G1, G2, and S in cells treated with 200 μmol/L H2O2 and various concentrations of TSM and cumulative data from three independent experiments were shown.

Mentions: From the cell cycle analysis, we found that when the control group (G1 phase: 49%; G2 phase: 5%; S phase: 46%) was compared with the H2O2 group the cells at G1 phase reduced to 40.33% and the cells at S phase increased to 54.67%. After cotreatment with various concentrations of TSM and when compared with the H2O2 group, the G1 phase cells rate increased to 41.67% (0.05 mg/mL TSM group), 42.67% (0.5 mg/mL TSM group), and 47.67% (5 mg/mL TSM group), respectively; these three groups were higher than the H2O2 group. But for the S phase, the cells rate recovered to 53.33% (0.05 mg/mL TSM group), 52.33% (0.5 mg/mL TSM group), and 47.33% (5 mg/mL TSM group), lower than the H2O2 group, referring to Figure 7. The results revealed that in the H2O2 group the cell cycle was terminated at S phase; when adding the various concentrations of TSM we confirmed that it could attenuate this phenomenon.


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)

The cell cycle modifications induced by TSM. (a) Control group. The cells were treated with 200 μmol/L H2O2 (b) and 0.05, 0.5, and 5 mg/mL TSM in the presence of 200 μmol/L H2O2 ((c), (d), and (e)). The blue color represented the diploid G1 phase; the red color represented the diploid G2 phase; and the grey color represented the diploid S phase. The percentage of G1, G2, and S in cells treated with 200 μmol/L H2O2 and various concentrations of TSM and cumulative data from three independent experiments were shown.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig7: The cell cycle modifications induced by TSM. (a) Control group. The cells were treated with 200 μmol/L H2O2 (b) and 0.05, 0.5, and 5 mg/mL TSM in the presence of 200 μmol/L H2O2 ((c), (d), and (e)). The blue color represented the diploid G1 phase; the red color represented the diploid G2 phase; and the grey color represented the diploid S phase. The percentage of G1, G2, and S in cells treated with 200 μmol/L H2O2 and various concentrations of TSM and cumulative data from three independent experiments were shown.
Mentions: From the cell cycle analysis, we found that when the control group (G1 phase: 49%; G2 phase: 5%; S phase: 46%) was compared with the H2O2 group the cells at G1 phase reduced to 40.33% and the cells at S phase increased to 54.67%. After cotreatment with various concentrations of TSM and when compared with the H2O2 group, the G1 phase cells rate increased to 41.67% (0.05 mg/mL TSM group), 42.67% (0.5 mg/mL TSM group), and 47.67% (5 mg/mL TSM group), respectively; these three groups were higher than the H2O2 group. But for the S phase, the cells rate recovered to 53.33% (0.05 mg/mL TSM group), 52.33% (0.5 mg/mL TSM group), and 47.33% (5 mg/mL TSM group), lower than the H2O2 group, referring to Figure 7. The results revealed that in the H2O2 group the cell cycle was terminated at S phase; when adding the various concentrations of TSM we confirmed that it could attenuate this phenomenon.

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