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Drug: Propofol

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Total 35 results found since Jan 2013.

Role of MnSOD in propofol protection of human umbilical vein endothelial cells injured by heat stress
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.
Source: Journal of Anesthesia - January 13, 2016 Category: Anesthesiology Source Type: research

Propofol inhibits growth and invasion of pancreatic cancer cells through regulation of the miR-21/Slug signaling pathway.
CONCLUSIONS: Propofol can effectively inhibit invasion and induce apoptosis of PANC-1 cells by regulating miR-21/Slug signals. PMID: 27829997 [PubMed - in process]
Source: American Journal of Translational Research - November 12, 2016 Category: Research Tags: Am J Transl Res Source Type: research

Propofol Suppresses Esophageal Squamous Cell Carcinoma Cell Migration and Invasion by Down-Regulation of Sex-Determining Region Y-box 4 (SOX4).
CONCLUSIONS Propofol inhibits EC9706 cell migration and invasion by down-regulation of SOX4. PMID: 28118321 [PubMed - in process]
Source: Medical Science Monitor - January 25, 2017 Category: Research Tags: Med Sci Monit Source Type: research

Propofol induces apoptosis of non-small cell lung cancer cells via ERK1/2-dependent upregulation of PUMA.
CONCLUSIONS: Propofol inhibits viability and induces apoptosis of A549 cells via an ERK1/2-dependent PUMA signaling. PMID: 30024623 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - July 20, 2018 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Propofol attenuates TNF- α-induced MMP-9 expression in human cerebral microvascular endothelial cells by inhibiting Ca2+/CAMK II/ERK/NF-κB signaling pathway.
In conclusion, propofol inhibits TNF-α-induced MMP-9 expression in hCMEC/D3 cells via repressing the Ca2+/CAMKII/ERK/NF-κB signaling pathway. TNF-α-impaired BBB integrity could be reversed by propofol, and propofol attenuates the inhibitory effect of TNF-α on collagen IV. PMID: 31235816 [PubMed - as supplied by publisher]
Source: Acta Pharmacologica Sinica - June 23, 2019 Category: Drugs & Pharmacology Authors: Ding XW, Sun X, Shen XF, Lu Y, Wang JQ, Sun ZR, Miao CH, Chen JW Tags: Acta Pharmacol Sin Source Type: research

Propofol Induces Cardioprotection Against Ischemia-Reperfusion Injury via Suppression of Transient Receptor Potential Vanilloid 4 Channel
Ca2+ entry via the transient receptor potential vanilloid 4 (TRPV4) channel contributes to Ca2+ overload and triggers many pathophysiological conditions, including myocardial ischemia/reperfusion (I/R) injury. Propofol, a widely used intravenous anesthetic, attenuates myocardial I/R injury. However, the mechanism of propofol remains to be examined. The present study aims to test the hypothesis that propofol attenuates myocardial I/R injury through the suppression of TRPV4. We used a murine ex vivo model of myocardial I/R and in vitro cultured myocytes subjected to hypoxia/reoxygenation (H/R). Propofol or TRPV4 antagonist, ...
Source: Frontiers in Pharmacology - October 3, 2019 Category: Drugs & Pharmacology Source Type: research

Propofol Affects Non-Small-Cell Lung Cancer Cell Biology By Regulating the miR-21/PTEN/AKT Pathway In Vitro and In Vivo.
CONCLUSIONS: Our study indicated that propofol inhibited A549 cell growth, accelerated apoptosis via the miR-21/PTEN/AKT pathway in vitro, suppressed NSCLC tumor cell growth, and promoted apoptosis in vivo. Our findings provide new implications for propofol in cancer therapy and indicate that propofol is extremely advantageous in surgical treatment. PMID: 32925348 [PubMed - in process]
Source: Anesthesia and Analgesia - September 16, 2020 Category: Anesthesiology Authors: Zheng X, Dong L, Zhao S, Li Q, Liu D, Zhu X, Ge X, Li R, Wang G Tags: Anesth Analg Source Type: research

Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
ConclusionIt is concluded that propofol postconditioning attenuated H9c2 cardiac cells apoptosis and autophagy induced by H/R injury through upregulating FoxO1 and FoxO3a under hyperglycemia.
Source: Military Medical Research - November 10, 2021 Category: International Medicine & Public Health Source Type: research

lncRNA BDNF-AS Attenuates Propofol-Induced Apoptosis in HT22 Cells by Modulating the BDNF/TrkB Pathway
This study aimed to investigate the involvement of BDNF-AS in propofol-induced apoptosis in HT22 cells. HT22 cells were treated with various concentrations of propofol at different time points. BDNF-AS was silenced using BDNF-AS-targeting siRNA. TrkB was antagonized by the TrkB inhibitor, ANA-12. Flow cytometry, quantitative reverse-transcription PCR, and western blotting were performed to analyze apoptosis and the expression of genes and proteins, respectively. In propofol-treated HT22 cells, BDNF-AS was upregulated, and BDNF was downregulated in a time- and dose-dependent manner. BDNF-AS downregulation mediated by siRNA ...
Source: Molecular Neurobiology - March 26, 2022 Category: Neurology Source Type: research

Endoplasmic Reticulum Stress is Involved in the Neuroprotective Effect of Propofol.
In this study, we found that propofol up-regulated BiP and attenuated tunicamycin-induced neural cell death. Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP). We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6. However, pretreatment with propofol attenuated the levels of phosphorylated protein kinase receptor-like ER kinase, phosphorylated elF2α, ATF4, and caspase-3, but failed to affect the increase of cleaved ATF6 and XBP1s, induced by tunicamyci...
Source: Neurochemical Research - June 25, 2014 Category: Neuroscience Authors: Wang L, Tang W, Jiang T, Lu P, Li Y, Sun A, Shen Y, Chen Y, Wang H, Zong Z, Wang Y, Chen L, Shen Y Tags: Neurochem Res Source Type: research

Propofol Attenuates Lipopolysaccharide-Induced Reactive Oxygen Species Production Through Activation of Nrf2/GSH and Suppression of NADPH Oxidase in Human Alveolar Epithelial Cells
In conclusion, propofol reduced LPS-induced ROS production via inhibition of inflammatory factors and enhancement of Nrf2-related antioxidant defense, providing its cytoprotective evidence under inflammatory conditions.
Source: Inflammation - October 23, 2014 Category: Biomedical Science Source Type: research