scholarly journals The protective effect of selenium from heat stress-induced porcine small intestinal epithelial cell line (IPEC-J2) injury is associated with regulation expression of selenoproteins

2019 ◽  
Vol 122 (10) ◽  
pp. 1081-1090
Author(s):  
Jiayong Tang ◽  
Lei Cao ◽  
Gang Jia ◽  
Guangmang Liu ◽  
Xiaoling Chen ◽  
...  
Keyword(s):  
Heat Stress ◽  
Protective Effect ◽  
Cell Viability ◽  
Cell Injury ◽  
Negative Impact ◽  
Cellular Damage ◽  
Epithelial Cell Line ◽  
Glutathione Peroxidase 1 ◽  
Protein Levels ◽  
Encoding Genes

AbstractThe present study compared the protective effect of sodium selenite (SS) and selenomethionine (SeMet) on heat stress (HS)-invoked porcine IPEC-J2 cellular damage and integrate potential roles of corresponding selenoprotein. Cells were cultured at 37°C until 80 % confluence and then subjected to four different conditions for 24 h: at 37°C (control), 41·5°C (HS), 41·5°C supplied with 0·42 µmol Se/L SS (SS), or SeMet (SeMet). HS significantly decreased cell viability, up-regulated mRNA and protein levels of heat shock protein 70 (HSP70) and down-regulated mRNA and protein levels of tight junction-related proteins (claudin-1 (CLDN-1) and zonula occludens-1 (ZO-1)). HS-induced cell injury was associated with the up-regulation (P < 0·05) of six inflammation-related genes and fourteen selenoprotein encoding genes and down-regulation (P < 0·05) of two inflammation-related genes and five selenoprotein encoding genes. Compared with the HS group, SS and SeMet supplementation resulted in an increase (P < 0·05) in cell viability, decreased (P < 0·05) mRNA expression of HSP70 and six inflammation-related genes and rescue (P < 0·05) of mRNA and protein levels of CLDN-1 and ZO-1. SS and SeMet supplementation changes the expressions of nineteen selenoprotein encoding genes in cells affected by HS. Both Se supplementation significantly recovered the protein level of glutathione peroxidase-1 and increased selenoprotein P in the IPEC-J2 cells under HS, respectively. In summary, Se supplementation alleviated the negative impact of HS on IPEC-J2 cells, and their cellular protective effect was associated with regulation expression of selenoproteins, and SeMet exhibited a better protective effect.

scholarly journals Selenogenome and AMPK signal insight into the protective effect of dietary selenium on chronic heat stress-induced hepatic metabolic disorder in growing pigs

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yan Liu ◽  
Jiayong Tang ◽  
Ying He ◽  
Gang Jia ◽  
Guangmang Liu ◽  
...  
Keyword(s):  
Heat Stress ◽  
Protective Effect ◽  
Metabolic Disorder ◽  
Glycogen Content ◽  
Basal Diet ◽  
Liver Weight ◽  
Growing Pigs ◽  
Aberrant Expression ◽  
Protein Levels ◽  
Encoding Genes

Abstract Background Chronic heat stress (CHS) disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs. Selenium (Se) may regulate the metabolic state through affect selenoprotein. Thus, we investigate the protective effect of dietary hydroxy-4-methylselenobutanoic acid (HMSeBA) on CHS induced hepatic metabolic disorder in growing pigs, and the corresponding response of selenoprotein. Methods Forty crossbreed growing pigs were randomly assigned to five groups: control group raised in the thermoneutral environment (22 ± 2 °C) with basal diet; four CHS groups raised in hyperthermal condition (33 ± 2 °C) with basal diet and supplied with 0.0, 0.2, 0.4, and 0.6 mg Se/kg HMSeBA, respectively. The trial lasted 28 d. The serum biochemical, hepatic metabolism related enzyme, protein and gene expression and 25 selenoproteins in liver tissue were determined by real-time PCR, ELISA and western blot. Results CHS significantly increased the rectal temperature, respiration rate, serum aspartate aminotransferase (AST) and low-density lipoprotein cholesterol (LDL-C) of pigs, up-regulated hepatic heat shock protein 70 (HSP70) and induced lower liver weight, glycogen content, hepatic glucokinase and glutathione peroxidase (GSH-Px). The CHS-induced liver metabolic disorder was associated with the aberrant expression of 6 metabolism-related gene and 11 selenoprotein encoding genes, and decreased the protein abundance of GCK, GPX4 and SELENOS. HMSeBA improved anti-oxidative capacity of liver. 0.4 or 0.6 mg Se/kg HMSeBA supplementation recovered the liver weight, glycogen content and rescue of mRNA abundance of genes related to metabolism and protein levels of GCK. HMSeBA supplementation changed expressions of 15 selenoprotein encoding genes, and enhanced protein expression of GPX1, GPX4 and SELENOS in the liver affected by CHS. CHS alone showed no impact while HMSeBA supplementation increased protein levels of p-AMPKα in the liver. Conclusions In summary, HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder, recovered the liver glycogen content and the processes that are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.

scholarly journals Selenogenome and AMPK signal insight into the protective effect of dietary Se on chronic heat stress-induced hepatic metabolic disorder in growing pigs

2021 ◽  
Author(s):  
Yan Liu ◽  
Jiayong Tang ◽  
Ying He ◽  
Gang Jia ◽  
Guangmang Liu ◽  
...  
Keyword(s):  
Heat Stress ◽  
Protective Effect ◽  
Metabolic Disorder ◽  
Glycogen Content ◽  
Basal Diet ◽  
Liver Weight ◽  
Growing Pigs ◽  
Aberrant Expression ◽  
Protein Levels ◽  
Encoding Genes

Abstract Background:Chronic heat stress (CHS) disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs. Selenium (Se) may regulate the metabolic state through affect selenoprotein. Thus, we investigate the protective effect of dietary hydroxy-4-methylselenobutanoic acid (HMSeBA) on CHS induced hepatic metabolic disorder in growing pigs, and the corresponding response of selenoprotein. Methods:Forty crossbreed growing pigs were randomly assigned to five groups: control group raised in the thermoneutral environment (22 ± 2 oC) with basal diet; four CHS groups raised in hyperthermal condition (33 ± 2 oC) with basal diet and supplied with 0.0, 0.2, 0.4 and 0.6 mg Se/kg HMSeBA, respectively. The trial lasted 28 days. The serum biochemical, hepatic metabolism related enzyme, protein and gene expression and 25 selenoproteins in liver tissue were determined by real-time PCR, ELISA and western blot.Results:CHS significantly increased the rectal temperature, respiration rate, serum aspartate aminotransferase (AST) and low-density lipoprotein cholesterol (LDL-C) of pigs, up-regulated hepatic heat shock protein 70 (HSP70) and induced lower liver weight, glycogen content, hepatic glucokinase and glutathione peroxidase (GSH-Px). The CHS-induced liver metabolic disorder was associated with the aberrant expression of 6 metabolism-related gene and 11 selenoprotein encoding genes, and decreased the protein abundance of GCK, GPX4 and SELENOS. HMSeBA improved anti-oxidative capacity of liver. 0.4 or 0.6 mg Se/kg HMSeBA supplementation recovered the liver weight, glycogen content and rescue of mRNA abundance of genes related to metabolism and protein levels of GCK. HMSeBA supplementation changed expressions of 15 selenoprotein encoding genes, and enhanced protein expression of GPX1, GPX4 and SELENOS in the liver affected by CHS. CHS alone showed no impact while HMSeBA supplementation increased protein levels of p-AMPKα in the liver. Conclusions:In summary, HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder, recovered the liver glycogen content and the processes are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.

scholarly journals Selenogenome and AMPK signal insight into the protective effect of dietary Se on chronic heat-stress induced hepatic metabolic disorder in growing pigs

2020 ◽  
Author(s):  
Yan Liu ◽  
Jiayong Tang ◽  
Ying He ◽  
Gang Jia ◽  
Guangmang Liu ◽  
...  
Keyword(s):  
Heat Stress ◽  
Protective Effect ◽  
Metabolic Disorder ◽  
Basal Diet ◽  
Liver Weight ◽  
Growing Pigs ◽  
Control Group ◽  
Aberrant Expression ◽  
Protein Levels ◽  
Encoding Genes

Abstract Background:Chronic heat stress (CHS) disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs. Selenium (Se) may regulate the metabolic state through affect selenoprotein. Thus, we investigate the protective effect of dietary hydroxy-4-methylselenobutanoic acid (HMSeBA) on CHS induced hepatic metabolic disorder in growing pigs, and the corresponding response of selenoprotein. Methods:Forty crossbreed growing pigs were randomly assigned to five groups: control group raised in the thermoneutral environment (22 ± 2 oC) with basal diet; four CHS groups raised in hyperthermal condition (33 ± 2 oC) with basal diet and supplied with 0.0, 0.2, 0.4 and 0.6 mg Se/kg HMSeBA, respectively. The trial lasted 28 days. Results:CHS significantly increased the rectal temperature, respiration rate, serum aspartate aminotransferase (AST) and low-density lipoprotein cholesterol (LDL-C) of pigs, up-regulated hepatic heat shock protein 70 (HSP70) and induced lower liver weight, hepatic glucokinase and glutathione peroxidase (GSH-Px). The CHS-induced liver metabolic disorder was associated with the aberrant expression of 6 metabolism-related gene and 11 selenoprotein encoding genes, and decreased the protein abundance of GCK, GPX4 and SELENOS. HMSeBA supplementation recovered the liver weight and improved anti-oxidative capacity and metabolism function in the liver. 0.4 or 0.6 mg Se/kg HMSeBA rescue of mRNA abundance of genes related to metabolism and protein levels of GCK. HMSeBA supplementation changed expressions of 15 selenoprotein encoding genes, and enhanced protein expression of GPX1, GPX4 and SELENOS in the liver affected by CHS. CHS alone showed no impact while HMSeBA supplementation increased protein levels of p-AMPKα in the liver. Conclusions:In summary, HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder, and the processes are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.

scholarly journals Protective Effect and Mechanism of Total Flavones fromRhododendron simsiiPlanch Flower on Cultured Rat Cardiomyocytes with Anoxia and Reoxygenation

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Yi Jiao ◽  
Yi-Fei Fan ◽  
Yu-Ling Wang ◽  
Jun-Yan Zhang ◽  
Shuo Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Protective Effect ◽  
Cell Viability ◽  
Ischemia Reperfusion ◽  
Cellular Damage ◽  
Protective Mechanism ◽  
Patch Clamp Technique ◽  
Rat Cardiomyocytes ◽  
Whole Cell Patch Clamp ◽  
Myocardial Ischemia Reperfusion

Many flavonoids have cardioprotection against myocardial ischemia/reperfusion (I/R) injury. Total flavones fromRhododendron simsiiPlanch flower (TFR) can protect myocardial ischemic injuries. However, its protective mechanism is still unknown. The present study was designed to investigate the mechanism of TFR on myocardial I/R and anoxia/reoxygenation (A/R) injuries. Rat model of myocardial I/R injury was made, and myocardial infarction was determined. A/R injury was induced in cultured rat cardiomyocytes; cellular damage was evaluated by measuring cell viability, LDH and cTnT releases, and MDA content. Expressions of ROCK1and ROCK2protein were examined by Western blot analysis, and K+currents were recorded by using whole-cell patch clamp technique. TFR 20~80 mg/kg markedly reduced I/R-induced myocardial infarction. TFR 3.7~300 mg/L significantly inhibited A/R-induced reduction of cell viability, LDH and cTnT releases, and MDA production. Exposure to A/R significantly increased ROCK1and ROCK2expressions in rat cardiomyocytes, but TFR 33.3~300 mg/L obviously inhibited this increase. 300 mg/L TFR significantly augmented inward rectifier K+current and other K+currents in rat cardiomyocytes. These results indicate that TFR has a protective effect on rat cardiomyocytes A/R damage, and the protective mechanism may be engaged with the inhibition of ROCK1and ROCK2and activation of K+channels.

scholarly journals Ganoderma lucidum Polysaccharides Prevent Palmitic Acid-Evoked Apoptosis and Autophagy in Intestinal Porcine Epithelial Cell Line via Restoration of Mitochondrial Function and Regulation of MAPK and AMPK/Akt/mTOR Signaling Pathway

2019 ◽  
Vol 20 (3) ◽  
pp. 478 ◽  
Author(s):  
Zengenni Liang ◽  
Zhihang Yuan ◽  
Jiajing Guo ◽  
Jing Wu ◽  
Jine Yi ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Protective Effect ◽  
Palmitic Acid ◽  
Cell Line ◽  
Mitochondrial Function ◽  
Ganoderma Lucidum ◽  
Cell Injury ◽  
Biologically Active ◽  
Epithelial Cell Line

Ganoderma lucidum polysaccharide (GLP) extracted from Ganoderma lucidum (Leyss. ex Fr.) Karst, a traditional Chinese medicine, is a biologically active substance reported to possess anti-oxidative, anti-apoptotic, and neurological protection. However, it is unknown whether GLP have any protective effect against high-fat constituents-induced epithelial cell injury. The aim of this study was to investigate the protection and molecular mechanism of GLP on injury induced by palmitic acid (PA) in the intestinal porcine epithelial cell line (IPEC-J2). First, we tested whether the treatment of GLP attenuate PA-induced IPEC-J2 cell death. GLP markedly blocked PA-caused cytotoxicity and apoptosis in IPEC-J2 cells. Moreover, GLP recovered the decreased mitochondrial function and inhibited activation of caspase-dependent apoptotic pathway. Interestingly, PA promoted cell apoptosis and autophagy through stimulation of phosphorylation of mitogen-activated protein kinases (MAPKs), AMP-activated protein kinase (AMPK), and inhibition of phosphorylation of Akt and mammalian target of rapamycin (mTOR), which was reversed by GLP. Taken together, this study revealed a protective effect of GLP against PA-evoked IPEC-J2 cell death through anti-apoptotic and anti-autophagic properties.

scholarly journals 1,8-cineol attenuated Aβ25-35-induced neuron injury through inhibiting IL-6, IL-8 release and NF-κB expression

2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Changliang Lu ◽  
Lin Wang ◽  
Shumei Wang ◽  
Wanzhong Li ◽  
Haijian Li ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cell Viability ◽  
Western Blotting ◽  
Cortical Neurons ◽  
Cell Injury ◽  
Neuronal Cells ◽  
Rat Cortical Neurons ◽  
Induced Neuron ◽  
Neuron Injury

Objective: To explore the protective effect of 1,8-cineol against Amyloid beta25-35 ( Aβ25-35)-induced cell injury in primary rat cortical neurons. Methods: Primary rat cortical neurons were cultured in vitro, treated with different concentrations of Aβ25-35 (2.5, 5, 10 20, 40 μM) and 1,8-cineol (1, 3, 10 μM). Cell viability of neuronal cells were detected by MTT assay and cell death were detected by lactate dehydrogenase release (LDH). The production of IL-6 and IL-8 in the supernatant were measured by ELISA assay kits. NF-κB protein expression was detected by Western blotting. Results: In primary cultured neurons, Aβ25-35 concentration dependently reduced cell viability and increased LDH release. 1,8-cineol with concentrations of 3 and 10 μM protected neuronal cells against Aβ25-35 induced cell injury for 24 h. 3 and 10 μM of 1,8-cineol also significantly decreased the levels of IL-6 and IL-8 cytokine production in the supernatant. Increased NF-κB expression was also significantly reduced by 1,8-cineol treatment evaluated by Western blotting. Conclusions: Our results revealed a protective effect of 1,8-cineol on Aβ25-35 induced neuron injury through inhibition of IL-6, IL-8 production and NF-κB expression.

scholarly journals Protective Effect of Patchouli Alcohol Against SH-SY5Y Cell Injury Induced by Aβ25-35 via the Reduction of Oxidative Stress and Apoptosis

2021 ◽  
Vol 16 (7) ◽  
pp. 1934578X2110317
Author(s):  
Xie Yun-Liang ◽  
Zhang Bo
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Cell Injury ◽  
Lactic Dehydrogenase ◽  
Underlying Mechanism ◽  
Mtor Pathway ◽  
Protein Levels ◽  
Patchouli Alcohol ◽  
Injury Group ◽  
Phosphorylated Akt

Patchouli alcohol (PA) has multiple pharmacological activities, but its protective effect against SH-SY5Y cell injury induced by Aβ25-35 has not been reported. It has been recorded that phosphatidylinositol 3-hydroxykinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway plays an important role in neuroprotection. The purpose of this study was to investigate the protective effect of PA against SH-SY5Y cell injury induced by Aβ25-35 and its underlying mechanism. The results showed that compared with that in the Aβ25-35-induced injury group, the survival rate of SH-SY5Y cells increased ( P < .01) in the different PA-treated groups and the lactic dehydrogenase activity decreased significantly ( P < .01) in the 10, 20, and 40 μg/mL PA groups; compared with those in the Aβ25-35-induced injury group, the malonyldialdehyde contents in SH-SY5Y cells decreased ( P < .05 or P < .01), while the superoxide dismutase, glutathione peroxidase, and catalase activities increased significantly ( P < .05 or P < .01) in the different PA-treated groups; compared with those in the Aβ25-35-induced injury group, the apoptosis rates, and the mRNA and protein levels of Caspase-3 and Bax in SH-SY5Y cells decreased ( P < .05 or P < .01), while the mRNA and protein levels of Bcl-2, and phosphorylated Akt (p-Akt) and phosphorylated mTOR protein levels increased significantly ( P < .05 or P < .01) in the different PA-treated groups. The above results indicate that PA can inhibit the oxidative stress and apoptosis of SH-SY5Y cells induced by Aβ25-35 by regulating the PI3K/Akt/mTOR pathway, to protect the SH-SY5Y cells from the injury induced by Aβ25-35.

scholarly journals Induction of MicroRNA-24 by HIF-1 Protects Against Ischemic Injury in Rat Cardiomyocytes

2012 ◽  
pp. 555-565 ◽  
Author(s):  
D.-F. LI ◽  
J. TIAN ◽  
X. GUO ◽  
L.-M. HUANG ◽  
Y. XU ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Injury ◽  
Protective Role ◽  
Luciferase Reporter ◽  
Rat Cardiomyocytes ◽  
Protein Levels ◽  
Novel Treatment ◽  
Ldh Release ◽  
Apoptosis And Necrosis

MicroRNAs are emerging as important regulators of cardiac function. This study investigated the role of microRNA-24 (miR-24) in ischemic cardiomyocytes, based on the observation that miR-24 expression was significantly enhanced in the ischemic myocardium of rats. Using primary cultured rat cardiomyocytes, cell injury was induced by ischemic conditions, and the cells were evaluated for changes in lactate dehydrogenase (LDH) release, cell viability, apoptosis and necrosis. The results showed that miR-24 was increased in myocytes exposed to ischemia. When miR-24 was further overexpressed in ischemic myocytes using the mimic RNA sequence, LDH release was reduced, cell viability was enhanced, and apoptosis and necrosis rates were both decreased. By contrast, a deficiency in miR-24 resulted in the largest LDH release, lowest cell viability and highest apoptosis and necrosis rates in normal and ischemic myocytes, with significant changes compared to that of non-transfected myocytes. Additionally, the mRNA and protein levels of the pro-apoptotic gene, BCL2L11, were down-regulated by miR-24 overexpression and up-regulated by miR-24 deficiency. The luciferase reporter assay confirmed BCL2L11 to be a target of miR-24. Overall, this study showed a protective role for miR-24 against myocardial ischemia by inhibiting BCL2L11, and may represent a potential novel treatment for ischemic heart disease.

Saikosaponin-D Attenuates Heat Stress-Induced Oxidative Damage in LLC-PK1 Cells by Increasing the Expression of Anti-Oxidant Enzymes and HSP72

2014 ◽  
Vol 42 (05) ◽  
pp. 1261-1277 ◽  
Author(s):  
Bao-Zhen Zhang ◽  
Xiao-Tong Guo ◽  
Jian-Wei Chen ◽  
Yuan Zhao ◽  
Xia Cong ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Heat Stress ◽  
Oxidative Damage ◽  
Cellular Damage ◽  
Dependent Manner ◽  
Dna Ladder ◽  
Protein Levels ◽  
Zinc Superoxide Dismutase ◽  
Proximal Tubular ◽  
Anti Oxidant

Heat stress stimulates the production of reactive oxygen species (ROS), which cause oxidative damage in the kidney. This study clarifies the mechanism by which saikosaponin-d (SSd), which is extracted from the roots of Bupleurum falcatum L, protects heat-stressed pig kidney proximal tubular (LLC-PK1) cells against oxidative damage. SSd alone is not cytotoxic at concentrations of 1 or 3 μg/mL as demonstrated by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. To assess the effects of SSd on heat stress-induced cellular damage, LLC-PK1 cells were pretreated with various concentrations of SSd, heat stressed at 42°C for 1 h, and then returned to 37°C for 9 h. DNA ladder and MTT assays demonstrated that SSd helped to prevent heat stress-induced cellular damage when compared to untreated cells. Additionally, pretreatment with SSd increased the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) but decreased the concentration of malondialdehyde (MDA) in a dose-dependent manner when compared to controls. Furthermore, real-time PCR and Western blot analysis demonstrated that SSd significantly increased the expression of copper and zinc superoxide dismutase (SOD-1), CAT, GPx-1 and heat shock protein 72 (HSP72) at both the mRNA and protein levels. In conclusion, these results are the first to demonstrate that SSd ameliorates heat stress-induced oxidative damage by modulating the activity of anti-oxidant enzymes and HSP72 in LLC-PK1 cells.

scholarly journals Inhibition of Caveolae Contributes to Propofol Preconditioning-Suppressed Microvesicles Release and Cell Injury by Hypoxia-Reoxygenation

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Fan Deng ◽  
Shuang Wang ◽  
Shuyun Cai ◽  
Zhe Hu ◽  
Riping Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Membrane ◽  
Endothelial Cell ◽  
Cell Surface ◽  
Protective Effect ◽  
Cell Injury ◽  
Cellular Damage ◽  
Structural Protein ◽  
Surface Plasma ◽  
Antioxidative Stress

Endothelial microvesicles (EMVs), released after endothelial cell (EC) apoptosis or activation, may carry many adverse signals and propagate injury by intercellular transmission. Caveolae are 50–100 nm cell surface plasma membrane invaginations involved in many pathophysiological processes. Recent evidence has indicated EMVs and caveolae may have functional effects in cells undergoing H/R injury. Propofol, a widely used anaesthetic, confers antioxidative stress capability in the same process. But the connection between EMVs, H/R, and caveolae remains largely unclear. Here, we found that H/R significantly increased the release of EMVs, the expression of CAV-1 (the structural protein responsible for maintaining the shape of caveolae), oxidative stress, and the mitochondrial damage, and all these changes were inhibited by propofol preconditioning. Interestingly, the caveolae inhibitor Mβ-CD strengthened the protective effect of propofol preconditioning. We further found that the release of EMVs is more significantly reduced under propofol preconditioning in the presence of the caveolae inhibitor Mβ-CD. EMVs released from H/R-treated cells caused a substantially increased mitochondrial and cellular damage to normal HUVECs after 4 hours of coculture. Thus, we conclude that inhibition of caveolae contributes to propofol preconditioning-suppressed microvesicles release and cell injury by H/R.

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