TY  - JOUR
AU  - Prado, Yolanda
AU  - Echeverría, Cesar
AU  - Feijóo, Carmen G.
AU  - Riedel, Claudia A.
AU  - Cabello-Verrugio, Claudio
AU  - Santibanez, Juan F.
AU  - Simon, Felipe
PY  - 2023
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1296
AB  - Sepsis syndrome develops through enhanced secretion of pro-inflammatory cytokines and the generation of reactive oxygen species (ROS). Sepsis syndrome is characterized by vascular hyperpermeability, hypotension, multiple organ dysfunction syndrome (MODS), and increased mortality, among others. Endotoxemia-derived sepsis is an important cause of sepsis syndrome. During endotoxemia, circulating endotoxin interacts with endothelial cells (ECs), inducing detrimental effects on endothelium function. The endotoxin induces the conversion of ECs into fibroblasts, which are characterized by a massive change in the endothelial gene-expression pattern. This downregulates the endothelial markers and upregulates fibrotic proteins, mesenchymal transcription factors, and extracellular matrix proteins, producing endothelial fibrosis. Sepsis progression is modulated by the consumption of specific nutrients, including ω-3 fatty acids, ascorbic acid, and polyphenolic antioxidant flavonoids. However, the underlying mechanism is poorly described. The notion that gene expression is modulated during inflammatory conditions by nutrient consumption has been reported. However, it is not known whether nutrient consumption modulates the fibrotic endothelial gene-expression pattern during sepsis as a mechanism to decrease vascular hyperpermeability, hypotension, MODS, and mortality. Therefore, the aim of this study was to investigate the impact of the consumption of dietary ω-3 fatty acids, ascorbic acid, and polyphenolic antioxidant flavonoid supplements on the modulation of fibrotic endothelial gene-expression patterns during sepsis and to determine the effects on sepsis outcomes. Our results indicate that the consumption of supplements based on ω-3 fatty acids and polyphenolic antioxidant flavonoids was effective for improving endotoxemia outcomes through prophylactic ingestion and therapeutic usage. Thus, our findings indicated that specific nutrient consumption improves sepsis outcomes and should be considered in treatment.
PB  - MDPI
T2  - Antioxidants
T1  - Effect of Dietary Supplements with ω-3 Fatty Acids, Ascorbic Acid, and Polyphenolic Antioxidant Flavonoid on Gene Expression, Organ Failure, and Mortality in Endotoxemia-Induced Septic Rats
IS  - 3
SP  - 659
VL  - 12
DO  - 10.3390/antiox12030659
ER  - 

@article{
author = "Prado, Yolanda and Echeverría, Cesar and Feijóo, Carmen G. and Riedel, Claudia A. and Cabello-Verrugio, Claudio and Santibanez, Juan F. and Simon, Felipe",
year = "2023",
abstract = "Sepsis syndrome develops through enhanced secretion of pro-inflammatory cytokines and the generation of reactive oxygen species (ROS). Sepsis syndrome is characterized by vascular hyperpermeability, hypotension, multiple organ dysfunction syndrome (MODS), and increased mortality, among others. Endotoxemia-derived sepsis is an important cause of sepsis syndrome. During endotoxemia, circulating endotoxin interacts with endothelial cells (ECs), inducing detrimental effects on endothelium function. The endotoxin induces the conversion of ECs into fibroblasts, which are characterized by a massive change in the endothelial gene-expression pattern. This downregulates the endothelial markers and upregulates fibrotic proteins, mesenchymal transcription factors, and extracellular matrix proteins, producing endothelial fibrosis. Sepsis progression is modulated by the consumption of specific nutrients, including ω-3 fatty acids, ascorbic acid, and polyphenolic antioxidant flavonoids. However, the underlying mechanism is poorly described. The notion that gene expression is modulated during inflammatory conditions by nutrient consumption has been reported. However, it is not known whether nutrient consumption modulates the fibrotic endothelial gene-expression pattern during sepsis as a mechanism to decrease vascular hyperpermeability, hypotension, MODS, and mortality. Therefore, the aim of this study was to investigate the impact of the consumption of dietary ω-3 fatty acids, ascorbic acid, and polyphenolic antioxidant flavonoid supplements on the modulation of fibrotic endothelial gene-expression patterns during sepsis and to determine the effects on sepsis outcomes. Our results indicate that the consumption of supplements based on ω-3 fatty acids and polyphenolic antioxidant flavonoids was effective for improving endotoxemia outcomes through prophylactic ingestion and therapeutic usage. Thus, our findings indicated that specific nutrient consumption improves sepsis outcomes and should be considered in treatment.",
publisher = "MDPI",
journal = "Antioxidants",
title = "Effect of Dietary Supplements with ω-3 Fatty Acids, Ascorbic Acid, and Polyphenolic Antioxidant Flavonoid on Gene Expression, Organ Failure, and Mortality in Endotoxemia-Induced Septic Rats",
number = "3",
pages = "659",
volume = "12",
doi = "10.3390/antiox12030659"
}

Prado, Y., Echeverría, C., Feijóo, C. G., Riedel, C. A., Cabello-Verrugio, C., Santibanez, J. F.,& Simon, F.. (2023). Effect of Dietary Supplements with ω-3 Fatty Acids, Ascorbic Acid, and Polyphenolic Antioxidant Flavonoid on Gene Expression, Organ Failure, and Mortality in Endotoxemia-Induced Septic Rats. in Antioxidants
MDPI., 12(3), 659.
https://doi.org/10.3390/antiox12030659

Prado Y, Echeverría C, Feijóo CG, Riedel CA, Cabello-Verrugio C, Santibanez JF, Simon F. Effect of Dietary Supplements with ω-3 Fatty Acids, Ascorbic Acid, and Polyphenolic Antioxidant Flavonoid on Gene Expression, Organ Failure, and Mortality in Endotoxemia-Induced Septic Rats. in Antioxidants. 2023;12(3):659.
doi:10.3390/antiox12030659 .

Prado, Yolanda, Echeverría, Cesar, Feijóo, Carmen G., Riedel, Claudia A., Cabello-Verrugio, Claudio, Santibanez, Juan F., Simon, Felipe, "Effect of Dietary Supplements with ω-3 Fatty Acids, Ascorbic Acid, and Polyphenolic Antioxidant Flavonoid on Gene Expression, Organ Failure, and Mortality in Endotoxemia-Induced Septic Rats" in Antioxidants, 12, no. 3 (2023):659,
https://doi.org/10.3390/antiox12030659 . .

TY  - CHAP
AU  - Gatica, Sebastian
AU  - Aravena, Cristobal
AU  - Prado, Yolanda
AU  - Aravena, Diego
AU  - Echeverría, Cesar
AU  - Santibanez, Juan F.
AU  - Riedel, Claudia A.
AU  - Stehberg, Jimmy
AU  - Simon, Felipe
PY  - 2023
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1380
AB  - Dexmedetomidine is an adrenergic receptor agonist that has been regarded as neuroprotective in several studies without an objective measure to it. Thus, the aim of this meta-analysis was to analyze and quantify the current evidence for the neuroprotective effects of dexmedetomidine in animals. The search was performed by querying the National Library of Medicine. Studies were included based on their language, significancy of their results, and complete availability of data on animal characteristics and interventions. Risk of bias was assessed using SYRCLE’s risk of bias tool and certainty was assessed using the ARRIVE Guidelines 2.0. Synthesis was performed by calculating pooled standardized mean difference and presented in forest plots and tables. The number of eligible records included per outcome is the following: 22 for IL-1β, 13 for IL-6, 19 for apoptosis, 7 for oxidative stress, 7 for Escape Latency, and 4 for Platform Crossings. At the cellular level, dexmedetomidine was found protective against production of IL-1β (standardized mean difference (SMD) =  − 4.3 [− 4.8; − 3.7]) and IL-6 (SMD =  − 5.6 [− 6.7; − 4.6]), apoptosis (measured through TUNEL, SMD =  − 6.0 [− 6.8; − 4.6]), and oxidative stress (measured as MDA production, SMD =  − 2.0 [− 2.4; − 1.4]) exclusively in the central nervous system. At the organism level, dexmedetomidine improved behavioral outcomes measuring escape latency (SMD = − 2.4 [− 3.3; − 1.6]) and number of platform crossings (SMD = 9.1 [− 6.8; − 11.5]). No eligible study had high risk of bias and certainty was satisfactory for reproducibility in all cases. This meta-analysis highlights the complexity of adrenergic stimulation and sheds light into the mechanisms potentiated by dexmedetomidine, which could be exploited for improving current neuroprotective formulations.
PB  - Springer Nature
T2  - Advances in Molecular Pathology
T1  - Appraisal of the Neuroprotective Effect of Dexmedetomidine: A Meta-Analysis
EP  - 181
SP  - 163
DO  - 10.1007/978-3-031-26163-3_9
UR  - https://hdl.handle.net/21.15107/rcub_rimi_1380
ER  - 

@inbook{
author = "Gatica, Sebastian and Aravena, Cristobal and Prado, Yolanda and Aravena, Diego and Echeverría, Cesar and Santibanez, Juan F. and Riedel, Claudia A. and Stehberg, Jimmy and Simon, Felipe",
year = "2023",
abstract = "Dexmedetomidine is an adrenergic receptor agonist that has been regarded as neuroprotective in several studies without an objective measure to it. Thus, the aim of this meta-analysis was to analyze and quantify the current evidence for the neuroprotective effects of dexmedetomidine in animals. The search was performed by querying the National Library of Medicine. Studies were included based on their language, significancy of their results, and complete availability of data on animal characteristics and interventions. Risk of bias was assessed using SYRCLE’s risk of bias tool and certainty was assessed using the ARRIVE Guidelines 2.0. Synthesis was performed by calculating pooled standardized mean difference and presented in forest plots and tables. The number of eligible records included per outcome is the following: 22 for IL-1β, 13 for IL-6, 19 for apoptosis, 7 for oxidative stress, 7 for Escape Latency, and 4 for Platform Crossings. At the cellular level, dexmedetomidine was found protective against production of IL-1β (standardized mean difference (SMD) =  − 4.3 [− 4.8; − 3.7]) and IL-6 (SMD =  − 5.6 [− 6.7; − 4.6]), apoptosis (measured through TUNEL, SMD =  − 6.0 [− 6.8; − 4.6]), and oxidative stress (measured as MDA production, SMD =  − 2.0 [− 2.4; − 1.4]) exclusively in the central nervous system. At the organism level, dexmedetomidine improved behavioral outcomes measuring escape latency (SMD = − 2.4 [− 3.3; − 1.6]) and number of platform crossings (SMD = 9.1 [− 6.8; − 11.5]). No eligible study had high risk of bias and certainty was satisfactory for reproducibility in all cases. This meta-analysis highlights the complexity of adrenergic stimulation and sheds light into the mechanisms potentiated by dexmedetomidine, which could be exploited for improving current neuroprotective formulations.",
publisher = "Springer Nature",
journal = "Advances in Molecular Pathology",
booktitle = "Appraisal of the Neuroprotective Effect of Dexmedetomidine: A Meta-Analysis",
pages = "181-163",
doi = "10.1007/978-3-031-26163-3_9",
url = "https://hdl.handle.net/21.15107/rcub_rimi_1380"
}

Gatica, S., Aravena, C., Prado, Y., Aravena, D., Echeverría, C., Santibanez, J. F., Riedel, C. A., Stehberg, J.,& Simon, F.. (2023). Appraisal of the Neuroprotective Effect of Dexmedetomidine: A Meta-Analysis. in Advances in Molecular Pathology
Springer Nature., 163-181.
https://doi.org/10.1007/978-3-031-26163-3_9
https://hdl.handle.net/21.15107/rcub_rimi_1380

Gatica S, Aravena C, Prado Y, Aravena D, Echeverría C, Santibanez JF, Riedel CA, Stehberg J, Simon F. Appraisal of the Neuroprotective Effect of Dexmedetomidine: A Meta-Analysis. in Advances in Molecular Pathology. 2023;:163-181.
doi:10.1007/978-3-031-26163-3_9
https://hdl.handle.net/21.15107/rcub_rimi_1380 .

Gatica, Sebastian, Aravena, Cristobal, Prado, Yolanda, Aravena, Diego, Echeverría, Cesar, Santibanez, Juan F., Riedel, Claudia A., Stehberg, Jimmy, Simon, Felipe, "Appraisal of the Neuroprotective Effect of Dexmedetomidine: A Meta-Analysis" in Advances in Molecular Pathology (2023):163-181,
https://doi.org/10.1007/978-3-031-26163-3_9 .,
https://hdl.handle.net/21.15107/rcub_rimi_1380 .

TY  - CHAP
AU  - Gatica, Sebastian
AU  - Aravena, Diego
AU  - Echeverría, Cesar
AU  - Santibanez, Juan F.
AU  - Riedel, Claudia A.
AU  - Simon, Felipe
PY  - 2023
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1390
AB  - Catecholamine stimulation over adrenergic receptors results in a state of hypercoagulability. Chronic stress involves the release and increase in circulation of catecholamines and other stress related hormones. Numerous observational studies in human have related stressful scenarios to several coagulation variables, but controlled stimulation with agonists or antagonists to adrenergic receptors are scarce. This systematic review is aimed at presenting an updated appraisal of the effect of adrenergic receptor modulation on variables related to human hemostasis by systematically reviewing the effect of adrenergic receptor-targeting drugs on scale variables related to hemostasis. By searching 3 databases for articles published between January 1st 2011 and February 16th, 2022 reporting effects on coagulation parameters from stimulation with α- or β-adrenergic receptor targeting drugs in humans regardless of baseline condition, excluding records different from original research and those not addressing the main aim of this systematic review. Risk of bias assessed using the Revised Cochrane risk-of-bias tool for randomized trials (RoB 2). Tables describing a pro-thrombotic anti-fibrinolytic state induced after β-adrenergic receptor agonist stimulation and the opposite after α1-, β-adrenergic receptor antagonist stimulation were synthesized from 4 eligible records by comparing hemostasis-related variables to their baseline. Notwithstanding this low number of records, experimental interventions included were sound and mostly unbiased, results were coherent, and outcomes were biologically plausible. In summary, this systematic review provides a critical systematic assessment and an updated elaboration, and its shortcomings highlight the need for further investigation in the field of hematology.
PB  - Springer Nature
T2  - Advances in Molecular Pathology
T2  - Advances in Molecular Pathology
T1  - Effects of Adrenergic Receptor Stimulation on Human Hemostasis: A Systematic Review
EP  - 63
SP  - 49
DO  - 10.1007/978-3-031-26163-3_3
ER  - 

@inbook{
author = "Gatica, Sebastian and Aravena, Diego and Echeverría, Cesar and Santibanez, Juan F. and Riedel, Claudia A. and Simon, Felipe",
year = "2023",
abstract = "Catecholamine stimulation over adrenergic receptors results in a state of hypercoagulability. Chronic stress involves the release and increase in circulation of catecholamines and other stress related hormones. Numerous observational studies in human have related stressful scenarios to several coagulation variables, but controlled stimulation with agonists or antagonists to adrenergic receptors are scarce. This systematic review is aimed at presenting an updated appraisal of the effect of adrenergic receptor modulation on variables related to human hemostasis by systematically reviewing the effect of adrenergic receptor-targeting drugs on scale variables related to hemostasis. By searching 3 databases for articles published between January 1st 2011 and February 16th, 2022 reporting effects on coagulation parameters from stimulation with α- or β-adrenergic receptor targeting drugs in humans regardless of baseline condition, excluding records different from original research and those not addressing the main aim of this systematic review. Risk of bias assessed using the Revised Cochrane risk-of-bias tool for randomized trials (RoB 2). Tables describing a pro-thrombotic anti-fibrinolytic state induced after β-adrenergic receptor agonist stimulation and the opposite after α1-, β-adrenergic receptor antagonist stimulation were synthesized from 4 eligible records by comparing hemostasis-related variables to their baseline. Notwithstanding this low number of records, experimental interventions included were sound and mostly unbiased, results were coherent, and outcomes were biologically plausible. In summary, this systematic review provides a critical systematic assessment and an updated elaboration, and its shortcomings highlight the need for further investigation in the field of hematology.",
publisher = "Springer Nature",
journal = "Advances in Molecular Pathology, Advances in Molecular Pathology",
booktitle = "Effects of Adrenergic Receptor Stimulation on Human Hemostasis: A Systematic Review",
pages = "63-49",
doi = "10.1007/978-3-031-26163-3_3"
}

Gatica, S., Aravena, D., Echeverría, C., Santibanez, J. F., Riedel, C. A.,& Simon, F.. (2023). Effects of Adrenergic Receptor Stimulation on Human Hemostasis: A Systematic Review. in Advances in Molecular Pathology
Springer Nature., 49-63.
https://doi.org/10.1007/978-3-031-26163-3_3

Gatica S, Aravena D, Echeverría C, Santibanez JF, Riedel CA, Simon F. Effects of Adrenergic Receptor Stimulation on Human Hemostasis: A Systematic Review. in Advances in Molecular Pathology. 2023;:49-63.
doi:10.1007/978-3-031-26163-3_3 .

Gatica, Sebastian, Aravena, Diego, Echeverría, Cesar, Santibanez, Juan F., Riedel, Claudia A., Simon, Felipe, "Effects of Adrenergic Receptor Stimulation on Human Hemostasis: A Systematic Review" in Advances in Molecular Pathology (2023):49-63,
https://doi.org/10.1007/978-3-031-26163-3_3 . .