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Conference Paper: Propofol enhances HO-1 expression and ameliorates hyperglycemia induced cardiomyocyte hypertrophy

TitlePropofol enhances HO-1 expression and ameliorates hyperglycemia induced cardiomyocyte hypertrophy
Authors
Issue Date2010
PublisherAmerican Society of Anesthesiologists. The Abstract Archive is located at http://www.asaabstracts.com/strands/asaabstracts/abstractArchive.htm
Citation
The 2010 Annual Meeting of the American Society of Anesthesiologists (ASA 2010), San Diego, CA., 16-20 October 2010. In Conference Proceedings, 2010, abstract no. 1409 How to Cite?
AbstractOBJECTIVE: Heme oxygenase-1(HO-1) is preferentially induced by stretch in cardiomyocytes[1], and can attenuate cardiac hypertrophy both in vivo and in vitro[2,3].High dose propofol treatment could attenuate postischemic reperfusion injury in the heart, kidney and brain partly through inducing mRNA and protein expression of HO-1.We hypothesized that propofol could ameliorate cardiomyocyte hypertrophy via the HO-1 pathway. METHODS: Primary cultured neonatal rat cardiomyocytes were exposed to a high concentration of glucose (HG, 25.5mmol/L) or normal glucose (5.5mmol/L, Control), HG in the presence of the HO-1 inducer cobalt protoporphyrin (CoPP) (10μM), the HO-1 inhibitor zinc protoporphyrin (ZnPP) (10μM), propofol (50 μM), propofol plus ZnPP or CoPP plus ZnPP, respectively, for 48 hours. Myocyte cross-sectional area was measured by immunocytochemical analysis. Myocyte protein content was determined by bicinchoninic acid assay. Reactive oxygen species (ROS) were detected by fluroescence of DCFA-DA staining. The levels of the lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD) were assayed by enzyme-liked immunosorbent assay. Reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis were used to detect HO-1 gene and protein expression. RESULTS: HG caused cardiomyocyte hypertrophy, manifest as significantly increased cardiomyocyte cross-sectional area and enhanced protein production, compared with control (all p < 0.01). This was accompanied by reduced HO-1 mRNA and protein expression (P<0.01, HG vs. control) and increased ROS and MDA production. CoPP and propofol, respectively, significantly increased HO-1 expression and attenuated HG-mediated cardiomyocyte hypertrophy, and reduced ROS and MDA production (p<0.05 or p<0.01). These protective effects of propofol or CoPP were abolished by ZnPP. CONCLUSIONS: Propofol ameliorates hyperglycemia induced cardiomyocyte hypertrophy, at least in part, by increasing HO-1 expression.
DescriptionTopic: Experimental Circulation: abstract no. A1409
Persistent Identifierhttp://hdl.handle.net/10722/140866

 

DC FieldValueLanguage
dc.contributor.authorXu, Jen_US
dc.contributor.authorXia, ZYen_US
dc.contributor.authorIrwin, MGen_US
dc.contributor.authorWong, GTCen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2011-09-23T06:20:27Z-
dc.date.available2011-09-23T06:20:27Z-
dc.date.issued2010en_US
dc.identifier.citationThe 2010 Annual Meeting of the American Society of Anesthesiologists (ASA 2010), San Diego, CA., 16-20 October 2010. In Conference Proceedings, 2010, abstract no. 1409en_US
dc.identifier.urihttp://hdl.handle.net/10722/140866-
dc.descriptionTopic: Experimental Circulation: abstract no. A1409-
dc.description.abstractOBJECTIVE: Heme oxygenase-1(HO-1) is preferentially induced by stretch in cardiomyocytes[1], and can attenuate cardiac hypertrophy both in vivo and in vitro[2,3].High dose propofol treatment could attenuate postischemic reperfusion injury in the heart, kidney and brain partly through inducing mRNA and protein expression of HO-1.We hypothesized that propofol could ameliorate cardiomyocyte hypertrophy via the HO-1 pathway. METHODS: Primary cultured neonatal rat cardiomyocytes were exposed to a high concentration of glucose (HG, 25.5mmol/L) or normal glucose (5.5mmol/L, Control), HG in the presence of the HO-1 inducer cobalt protoporphyrin (CoPP) (10μM), the HO-1 inhibitor zinc protoporphyrin (ZnPP) (10μM), propofol (50 μM), propofol plus ZnPP or CoPP plus ZnPP, respectively, for 48 hours. Myocyte cross-sectional area was measured by immunocytochemical analysis. Myocyte protein content was determined by bicinchoninic acid assay. Reactive oxygen species (ROS) were detected by fluroescence of DCFA-DA staining. The levels of the lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD) were assayed by enzyme-liked immunosorbent assay. Reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis were used to detect HO-1 gene and protein expression. RESULTS: HG caused cardiomyocyte hypertrophy, manifest as significantly increased cardiomyocyte cross-sectional area and enhanced protein production, compared with control (all p < 0.01). This was accompanied by reduced HO-1 mRNA and protein expression (P<0.01, HG vs. control) and increased ROS and MDA production. CoPP and propofol, respectively, significantly increased HO-1 expression and attenuated HG-mediated cardiomyocyte hypertrophy, and reduced ROS and MDA production (p<0.05 or p<0.01). These protective effects of propofol or CoPP were abolished by ZnPP. CONCLUSIONS: Propofol ameliorates hyperglycemia induced cardiomyocyte hypertrophy, at least in part, by increasing HO-1 expression.-
dc.languageengen_US
dc.publisherAmerican Society of Anesthesiologists. The Abstract Archive is located at http://www.asaabstracts.com/strands/asaabstracts/abstractArchive.htm-
dc.relation.ispartofProceedings of the 2010 Annual Meeting of the American Society Anesthesiologistsen_US
dc.titlePropofol enhances HO-1 expression and ameliorates hyperglycemia induced cardiomyocyte hypertrophyen_US
dc.typeConference_Paperen_US
dc.identifier.emailIrwin, MG: mgirwin@hkucc.hku.hken_US
dc.identifier.emailWong, GTC: gordon@hku.hken_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.identifier.authorityWong, GTC=rp00523en_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros193514en_US
dc.publisher.placeUnited States-
dc.customcontrol.immutablesml 130408-

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