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Drug: Propofol
Procedure: Anesthesia

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Total 21 results found since Jan 2013.

Propofol inhibits invasion and growth of ovarian cancer cells via regulating miR-9/NF- κB signal.
Propofol inhibits invasion and growth of ovarian cancer cells via regulating miR-9/NF-κB signal. Braz J Med Biol Res. 2016 Dec 12;49(12):e5717 Authors: Huang X, Teng Y, Yang H, Ma J Abstract Propofol is one of the most commonly used intravenous anesthetic agents during cancer resection surgery. A previous study has found that propofol can inhibit invasion and induce apoptosis of ovarian cancer cells. However, the underlying mechanisms are not known. miR-9 has been reported to be little expressed in ovarian cancer cells, which has been related to a poor prognosis in patients with ovarian cancer. Studie...
Source: Brazilian Journal of Medical and Biological Research - December 17, 2016 Category: Research Tags: Braz J Med Biol Res 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

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

Anesthetic agent propofol inhibits myeloid differentiation factor 88-dependent and independent signaling and mitigates lipopolysaccharide-mediated reactive oxygen species production in human neutrophils in vitro.
This study aimed to investigate the influence of PPF on lipopolysaccharide (LPS)-induced reactive oxygen species production in human neutrophils. We isolated neutrophils from the peripheral blood of 10 healthy male donors. Neither 1µg/ml LPS nor 10-150μmol/L PPF influenced the rate of neutrophil apoptosis, but PPF significantly inhibited LPS-mediated reactive oxygen species production in a dose-dependent manner. PPF inhibited LPS-induced expression of MyD88, tumor necrosis factor receptor-associated factor 6, and TRIF, but not the expression of interferon regulatory factor 3 or phosphorylation of p47(phox), p38-mitogen-a...
Source: European Journal of Pharmacology - October 28, 2014 Category: Drugs & Pharmacology Authors: Ren X, Lv F, Fang B, Liu S, Lv H, He G, Ma H, Cao Y, Wang Y Tags: Eur J Pharmacol 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

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