TY - JOUR
T1 - Coptis chinensis Franch. exhibits neuroprotective properties against oxidative stress in human neuroblastoma cells
AU - Friedemann, Thomas
AU - Otto, Benjamin
AU - Klätschke, Kristin
AU - Schumacher, Udo
AU - Tao, Yi
AU - Leung, Alexander Kai Man
AU - Efferth, Thomas
AU - Schröder, Sven
N1 - Funding Information:
This study was supported by the Innovationsstiftung Hamburg . The authors would like to thank PD Dr. M. Jendrach (Experimental Neurology, Department of Neurology, Goethe University Hospital, Frankfurt am Main, Germany) for the SH-SY5Y cells and Christine Knies (Institute of Anatomy and Experimental Morphology; University Medical Center Hamburg-Eppendorf, Hamburg, Germany) for her technological support. We also acknowledge Prof. Dr. C. Lohr (Division of Animal Physiology; University of Hamburg; Hamburg, Germany) for his support in form and content.
PY - 2014/8/8
Y1 - 2014/8/8
N2 - Ethnopharmacological relevance The dried rhizome of Coptis chinensis Franch. (family Ranunculaceae) is traditionally used in Chinese medicine for the treatment of inflammatory diseases and diabetes. Recent studies showed a variety of activities of Coptis chinensis Franch. alkaloids, including neuroprotective, neuroregenerative, anti-diabetic, anti-oxidative and anti-inflammatory effects. However, there is no report on the neuroprotective effect of Coptis chinensis Franch. watery extract against tert- butylhydroperoxide (t-BOOH) induced oxidative damage. The aim of the study is to investigate neuroprotective properties of Coptis chinensis Franch. rhizome watery extract (CRE) and to evaluate its potential mechanism of action. Materials and methods Neuroprotective properties on t-BOOH induced oxidative stress were investigated in SH-SY5Y human neuroblastoma cells. Cells were pretreated with CRE for 2 h or 24 h followed by 2 h of treatment with t-BOOH. To evaluate the neuroprotective effect of CRE, cell viability, cellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and the apoptotic rate were determined and microarray analyses, as well as qRT-PCR analyses were conducted. Results Two hours of exposure to 100 μM t-BOOH resulted in a significant reduction of cell viability, increased apoptotic rate, declined mitochondrial membrane potential (MMP) and increased ROS production. Reduction of cell viability, increased apoptotic rate and declined mitochondrial membrane potential (MMP) could be significantly reduced in cells pretreated with CRE (100 μg/ml) for 2 h or 24 h ahead of t-BOOH exposure with the greatest effect after 24 h of pretreatment; however ROS production was not changed significantly. Furthermore, microarray analyses revealed that the expressions of 2 genes; thioredoxin-interacting protein (TXNIP) and mitochondrially encoded NADH dehydrogenase 1, were significantly regulated. Down regulation of TXNIP was confirmed by qRT-PCR. Conclusion Due to its neuroprotective properties CRE might be a potential therapeutic agent for the prevention or amelioration of diseases like diabetic neuropathy and neurodegenerative disorders like Alzheimer and Parkinsons disease.
AB - Ethnopharmacological relevance The dried rhizome of Coptis chinensis Franch. (family Ranunculaceae) is traditionally used in Chinese medicine for the treatment of inflammatory diseases and diabetes. Recent studies showed a variety of activities of Coptis chinensis Franch. alkaloids, including neuroprotective, neuroregenerative, anti-diabetic, anti-oxidative and anti-inflammatory effects. However, there is no report on the neuroprotective effect of Coptis chinensis Franch. watery extract against tert- butylhydroperoxide (t-BOOH) induced oxidative damage. The aim of the study is to investigate neuroprotective properties of Coptis chinensis Franch. rhizome watery extract (CRE) and to evaluate its potential mechanism of action. Materials and methods Neuroprotective properties on t-BOOH induced oxidative stress were investigated in SH-SY5Y human neuroblastoma cells. Cells were pretreated with CRE for 2 h or 24 h followed by 2 h of treatment with t-BOOH. To evaluate the neuroprotective effect of CRE, cell viability, cellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and the apoptotic rate were determined and microarray analyses, as well as qRT-PCR analyses were conducted. Results Two hours of exposure to 100 μM t-BOOH resulted in a significant reduction of cell viability, increased apoptotic rate, declined mitochondrial membrane potential (MMP) and increased ROS production. Reduction of cell viability, increased apoptotic rate and declined mitochondrial membrane potential (MMP) could be significantly reduced in cells pretreated with CRE (100 μg/ml) for 2 h or 24 h ahead of t-BOOH exposure with the greatest effect after 24 h of pretreatment; however ROS production was not changed significantly. Furthermore, microarray analyses revealed that the expressions of 2 genes; thioredoxin-interacting protein (TXNIP) and mitochondrially encoded NADH dehydrogenase 1, were significantly regulated. Down regulation of TXNIP was confirmed by qRT-PCR. Conclusion Due to its neuroprotective properties CRE might be a potential therapeutic agent for the prevention or amelioration of diseases like diabetic neuropathy and neurodegenerative disorders like Alzheimer and Parkinsons disease.
KW - Apoptosis
KW - Coptidis rhizoma
KW - Neuroprotection
KW - Oxidative stress
KW - SH-SY5Y
KW - Thioredoxin-interacting protein
UR - http://www.scopus.com/inward/record.url?scp=84905114650&partnerID=8YFLogxK
U2 - 10.1016/j.jep.2014.06.004
DO - 10.1016/j.jep.2014.06.004
M3 - Journal article
C2 - 24929105
AN - SCOPUS:84905114650
SN - 0378-8741
VL - 155
SP - 607
EP - 615
JO - Journal of Ethnopharmacology
JF - Journal of Ethnopharmacology
IS - 1
ER -
