F Wu1, X J Dong2, H Q Zhang3, L Li4,5, Q L Xu6, Z F Liu6, Z T Gu7,8, L Su9. 1. Department of Nephrology, The Third People's Hospital of Zhengzhou, Zhengzhou, People's Republic of China. 2. Department of Hematology, The Third People's Hospital of Zhengzhou, Zhengzhou, People's Republic of China. 3. Department of Deratology, 421 Hospital of PLA, Guangzhou, People's Republic of China. 4. Department of Intensive Care Unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou, People's Republic of China. 5. Department of Pathophysiology, Southern Medical University, Guangzhou, 510515, People's Republic of China. 6. Department of Intensive Care Unit, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, General Hospital of Guangzhou Military Command, Guangzhou, People's Republic of China. 7. Department of Intensive Care Unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou, People's Republic of China. guzhengtao@126.com. 8. Department of Pathophysiology, Southern Medical University, Guangzhou, 510515, People's Republic of China. guzhengtao@126.com. 9. Department of Intensive Care Unit, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, General Hospital of Guangzhou Military Command, Guangzhou, People's Republic of China. sulei_icu@163.com.
Abstract
PURPOSE: Heat stress stimulation can cause various injuries in human umbilical vein endothelial cells (HUVEC), including apoptotic cell death and an increase in cell permeability. Propofol (PPF), a commonly used anesthetic, is known to have an important role in antioxidation as well as organ protection. Therefore, our aim is to evaluate the protective effects of PPF on heat stress (HS)-induced oxidative stress injury and its possible mechanism of action. METHODS: For HS + PPF, cells were treated with propofol followed by 2 h heat stress at 43 °C and then 4 h incubation under normal conditions. For propofol treatment, HUVEC were cultured in serum-free Dulbecco's modified Eagle medium supplemented with 0, 10, 25, or 50 μM propofol for 6 h under normal conditions. RESULTS: During the study, we found that, in HS-induced cellular damage, the protective effect of propofol was related closely with its antioxidation properties. We further revealed that heat stress significantly reduced the level of manganese superoxide demutase (MnSOD) and Cu/Zn SOD, but that propofol could inhibit the reduction of MnSOD only. Transfection of HUVEC with MnSOD small interfering RNA (siRNA) markedly decreased the expression of MnSOD, and the protective effect of propofol in the MnSOD siRNA clones was significantly reduced. CONCLUSION: Propofol protected the heat stress-injured cells, at least partly, through upregulating MnSOD expression, effectively reducing the direct or indirect cell damage caused by oxidative stress.
PURPOSE: Heat stress stimulation can cause various injuries in human umbilical vein endothelial cells (HUVEC), including apoptotic cell death and an increase in cell permeability. Propofol (PPF), a commonly used anesthetic, is known to have an important role in antioxidation as well as organ protection. Therefore, our aim is to evaluate the protective effects of PPF on heat stress (HS)-induced oxidative stress injury and its possible mechanism of action. METHODS: For HS + PPF, cells were treated with propofol followed by 2 h heat stress at 43 °C and then 4 h incubation under normal conditions. For propofol treatment, HUVEC were cultured in serum-free Dulbecco's modified Eagle medium supplemented with 0, 10, 25, or 50 μM propofol for 6 h under normal conditions. RESULTS: During the study, we found that, in HS-induced cellular damage, the protective effect of propofol was related closely with its antioxidation properties. We further revealed that heat stress significantly reduced the level of manganese superoxide demutase (MnSOD) and Cu/Zn SOD, but that propofol could inhibit the reduction of MnSOD only. Transfection of HUVEC with MnSOD small interfering RNA (siRNA) markedly decreased the expression of MnSOD, and the protective effect of propofol in the MnSOD siRNA clones was significantly reduced. CONCLUSION:Propofol protected the heat stress-injured cells, at least partly, through upregulating MnSOD expression, effectively reducing the direct or indirect cell damage caused by oxidative stress.
Entities:
Keywords:
Heat stress; Human umbilical vein endothelial cells; MnSOD; Propofol
Authors: Mark R Brinton; Chad A Tagge; Russell J Stewart; Alfred K Cheung; Yan-Ting E Shiu; Douglas A Christensen Journal: Int J Hyperthermia Date: 2012 Impact factor: 3.914
Authors: Maria Strassburger; Wilhelm Bloch; Silke Sulyok; Jutta Schüller; Alexander F Keist; Annette Schmidt; Jutta Wenk; Thorsten Peters; Meinhard Wlaschek; Jacek Lenart; Thomas Krieg; Martin Hafner; Angelika Kümin; Sabine Werner; Werner Müller; Karin Scharffetter-Kochanek Journal: Free Radic Biol Med Date: 2005-06-01 Impact factor: 7.376