Supplementary
-
Citations:
- Appears in Collections:
Conference Paper: Propofol enhances HO-1 expression and ameliorates hyperglycemia induced cardiomyocyte hypertrophy
Title | Propofol enhances HO-1 expression and ameliorates hyperglycemia induced cardiomyocyte hypertrophy |
---|---|
Authors | |
Issue Date | 2010 |
Publisher | American 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? |
Abstract | OBJECTIVE: 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. |
Description | Topic: Experimental Circulation: abstract no. A1409 |
Persistent Identifier | http://hdl.handle.net/10722/140866 |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Xu, J | en_US |
dc.contributor.author | Xia, ZY | en_US |
dc.contributor.author | Irwin, MG | en_US |
dc.contributor.author | Wong, GTC | en_US |
dc.contributor.author | Xia, Z | en_US |
dc.date.accessioned | 2011-09-23T06:20:27Z | - |
dc.date.available | 2011-09-23T06:20:27Z | - |
dc.date.issued | 2010 | en_US |
dc.identifier.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 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/140866 | - |
dc.description | Topic: Experimental Circulation: abstract no. A1409 | - |
dc.description.abstract | OBJECTIVE: 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.language | eng | en_US |
dc.publisher | American Society of Anesthesiologists. The Abstract Archive is located at http://www.asaabstracts.com/strands/asaabstracts/abstractArchive.htm | - |
dc.relation.ispartof | Annual Meeting of the American Society Anesthesiologists, ASA 2010 Proceedings | en_US |
dc.title | Propofol enhances HO-1 expression and ameliorates hyperglycemia induced cardiomyocyte hypertrophy | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Irwin, MG: mgirwin@hkucc.hku.hk | en_US |
dc.identifier.email | Wong, GTC: gordon@hku.hk | en_US |
dc.identifier.email | Xia, Z: zyxia@hkucc.hku.hk | en_US |
dc.identifier.authority | Irwin, MG=rp00390 | en_US |
dc.identifier.authority | Wong, GTC=rp00523 | en_US |
dc.identifier.authority | Xia, Z=rp00532 | en_US |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.hkuros | 193514 | en_US |
dc.publisher.place | United States | - |
dc.customcontrol.immutable | sml 130408 | - |