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Conference Paper: Propofol Ameliorates Hyperglycemia-induced Cardiac Hypertrophy and Dysfunction Via Heme Oxygenase-1 /STAT3 Signaling Pathway in Rats

TitlePropofol Ameliorates Hyperglycemia-induced Cardiac Hypertrophy and Dysfunction Via Heme Oxygenase-1 /STAT3 Signaling Pathway in Rats
Authors
Issue Date2014
PublisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.org
Citation
Annual Meeting of the International Anesthesia Research Society (IARS 2014), Montréal, Canada, 17-20 May 2014. In Anesthesia and Analgesia, 2014, v. 118 n. 5S, p. S-77 How to Cite?
AbstractINSTRUCTION AND GENERAL PURPOSE OF THE STUDY: Heme oxygenase-1 (HO-1) is inducible in cardiomyocytes in response to stimuli like oxidative stress, and plays critical roles in combating cardiac hypertrophy and injury1 .Signal transducer and activator of transcription-3(STAT3) plays a pivotal role in HO-1 mediated protection against liver and lung injury under oxidative stress2 . We hypothesized that propofol, an intravenous anesthetic with antioxidant capacity that has been shown to induce HO-1 expression, may attenuate hyperglycemia-induced oxidative stress in cardiomyocytes via enhancing HO-1 activation and ameliorate hyperglycemia-induced cardiac hypertrophy and apoptosis via HO-1 /STAT3 signaling, and improve cardiac function in diabetes. METHODS: 8 weeks of streptozotocin-induced Type 1diabetic rats received an i.v. injection of either saline or propofol at a UDWH RI ȝJ NJ PLQ3 for 45 min. Cardiac function was assayed by pressure-volume loop conduction system and free 15-F2tisoprostane in plasma and heart tissue was detected by enzymelinked immunoassay. Primary cultured neonatal rat cardiomyocytes were exposed for 48 hours to either normal glucose (5.5mmol.L-1, Control), a high concentration of glucose (HG, 25.5mmol.L-1) or +*LQWKHSUHVHQFHRISURSRIRO ȝPRO / 7RIXUWKHUFRQ¿UPWKH UROHVRI+2 DQG67$7 SODHGLQWKHEHQH¿FLDOHIIHFWVRISURSRIRO HO-1 or STAT3 genes expression was respectively knocked down by siRNA in H9c2 cells. Cardiomyocyte cross-sectional area and protein content were used as indices of hypertrophy. Reactive R[JHQVSHFLHV 526 ZHUHGHWHFWHGE'+(ÀXRUHVFHQFHVWDLQLQJ HO-1 and STAT3 protein expression were detected by Western blot. Cardiomyocytes apoptosis were assessed by TUNEL assay. RESULTS AND MAJOR FINDINGS: In Type-1 diabetic UDWV PRFDUGLDO ) W LVRSURVWDQH ZDV VLJQL¿FDQWO LQFUHDVHG accompanied with cardiomyocytes hypertrophy and impaired left ventricular function that was coincident with reduced HO-1 activity and STAT3 activation despite of an increase in HO-1 protein H[SUHVVLRQDVFRPSDUHGWRFRQWURO 3URSRIROLQIXVLRQVLJQL¿FDQWO improved cardiac function with concomitantly enhanced HO-1 activity and STAT3 activation. Similar to the changes seen in diabetic rat hearts, high glucose exposure for 48 hours led to cardiomyocytes hypertrophy and apoptosis in both the primarily cultured neonatal rat cardiomyocyte and in H9c2 cells compared to normal glucose, DFFRPSDQLHG E LQFUHDVHG 526 3URSRIRO VLJQL¿FDQWO LQFUHDVHG cardiomyocyte HO-1 and p-STAT3 protein expression and HO-1 activity and attenuated HG-mediated cardiomyocyte hypertrophy and apoptosis and reduced ROS production (P<0.05). These protective effects of propofol were abolished by HO-1 or STAT3 gene knock down in H9c2 cells. CONCLUSIONS: Activation of the HO-1/STAT3 signaling path way is major mechanism whereby Propofol mediates amelioration of hyperglycemia-induced cardiomyocyte hypertrophy and apoptosis and cardiac dysfunction. REFERENCES: 1 Circulation 2010;121:1912-25 2 J. of hepatology 2012;56:359-66) 3 BMC gastroenterology 2011;11:144
DescriptionSession: Cardiovascular Anesthesiology
The Abstract can be viewed at http://www.iars.org/assets/1/7/14AM_AbstractSupplement_051614.pdf
Persistent Identifierhttp://hdl.handle.net/10722/204765
ISSN
2015 Impact Factor: 3.827
2015 SCImago Journal Rankings: 1.523

 

DC FieldValueLanguage
dc.contributor.authorXu, Jen_US
dc.contributor.authorLi, Hen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2014-09-20T00:39:19Z-
dc.date.available2014-09-20T00:39:19Z-
dc.date.issued2014en_US
dc.identifier.citationAnnual Meeting of the International Anesthesia Research Society (IARS 2014), Montréal, Canada, 17-20 May 2014. In Anesthesia and Analgesia, 2014, v. 118 n. 5S, p. S-77en_US
dc.identifier.issn0003-2999-
dc.identifier.urihttp://hdl.handle.net/10722/204765-
dc.descriptionSession: Cardiovascular Anesthesiology-
dc.descriptionThe Abstract can be viewed at http://www.iars.org/assets/1/7/14AM_AbstractSupplement_051614.pdf-
dc.description.abstractINSTRUCTION AND GENERAL PURPOSE OF THE STUDY: Heme oxygenase-1 (HO-1) is inducible in cardiomyocytes in response to stimuli like oxidative stress, and plays critical roles in combating cardiac hypertrophy and injury1 .Signal transducer and activator of transcription-3(STAT3) plays a pivotal role in HO-1 mediated protection against liver and lung injury under oxidative stress2 . We hypothesized that propofol, an intravenous anesthetic with antioxidant capacity that has been shown to induce HO-1 expression, may attenuate hyperglycemia-induced oxidative stress in cardiomyocytes via enhancing HO-1 activation and ameliorate hyperglycemia-induced cardiac hypertrophy and apoptosis via HO-1 /STAT3 signaling, and improve cardiac function in diabetes. METHODS: 8 weeks of streptozotocin-induced Type 1diabetic rats received an i.v. injection of either saline or propofol at a UDWH RI ȝJ NJ PLQ3 for 45 min. Cardiac function was assayed by pressure-volume loop conduction system and free 15-F2tisoprostane in plasma and heart tissue was detected by enzymelinked immunoassay. Primary cultured neonatal rat cardiomyocytes were exposed for 48 hours to either normal glucose (5.5mmol.L-1, Control), a high concentration of glucose (HG, 25.5mmol.L-1) or +*LQWKHSUHVHQFHRISURSRIRO ȝPRO / 7RIXUWKHUFRQ¿UPWKH UROHVRI+2 DQG67$7 SODHGLQWKHEHQH¿FLDOHIIHFWVRISURSRIRO HO-1 or STAT3 genes expression was respectively knocked down by siRNA in H9c2 cells. Cardiomyocyte cross-sectional area and protein content were used as indices of hypertrophy. Reactive R[JHQVSHFLHV 526 ZHUHGHWHFWHGE'+(ÀXRUHVFHQFHVWDLQLQJ HO-1 and STAT3 protein expression were detected by Western blot. Cardiomyocytes apoptosis were assessed by TUNEL assay. RESULTS AND MAJOR FINDINGS: In Type-1 diabetic UDWV PRFDUGLDO ) W LVRSURVWDQH ZDV VLJQL¿FDQWO LQFUHDVHG accompanied with cardiomyocytes hypertrophy and impaired left ventricular function that was coincident with reduced HO-1 activity and STAT3 activation despite of an increase in HO-1 protein H[SUHVVLRQDVFRPSDUHGWRFRQWURO 3URSRIROLQIXVLRQVLJQL¿FDQWO improved cardiac function with concomitantly enhanced HO-1 activity and STAT3 activation. Similar to the changes seen in diabetic rat hearts, high glucose exposure for 48 hours led to cardiomyocytes hypertrophy and apoptosis in both the primarily cultured neonatal rat cardiomyocyte and in H9c2 cells compared to normal glucose, DFFRPSDQLHG E LQFUHDVHG 526 3URSRIRO VLJQL¿FDQWO LQFUHDVHG cardiomyocyte HO-1 and p-STAT3 protein expression and HO-1 activity and attenuated HG-mediated cardiomyocyte hypertrophy and apoptosis and reduced ROS production (P<0.05). These protective effects of propofol were abolished by HO-1 or STAT3 gene knock down in H9c2 cells. CONCLUSIONS: Activation of the HO-1/STAT3 signaling path way is major mechanism whereby Propofol mediates amelioration of hyperglycemia-induced cardiomyocyte hypertrophy and apoptosis and cardiac dysfunction. REFERENCES: 1 Circulation 2010;121:1912-25 2 J. of hepatology 2012;56:359-66) 3 BMC gastroenterology 2011;11:144-
dc.languageengen_US
dc.publisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.org-
dc.relation.ispartofAnesthesia and Analgesiaen_US
dc.rightsThis is a non-final version of an article published in final form in Anesthesia and Analgesia, 2014, v. 118 n. 5S, p. S-77-
dc.titlePropofol Ameliorates Hyperglycemia-induced Cardiac Hypertrophy and Dysfunction Via Heme Oxygenase-1 /STAT3 Signaling Pathway in Ratsen_US
dc.typeConference_Paperen_US
dc.identifier.emailXu, J: xushiwei@hku.hken_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.identifier.hkuros235604en_US
dc.identifier.volume118en_US
dc.identifier.issue5S-
dc.identifier.spageS-77en_US
dc.identifier.epageS-77en_US
dc.publisher.placeUnited States-

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