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Propofol protects hippocampal neurons from apoptosis in ischemic brain injury by increasing GLT-1 expression and inhibiting the activation of NMDAR via the JNK/Akt signaling pathway.
Abstract Ischemic brain injury (IBI) can cause nerve injury and is a leading cause of morbidity and mortality worldwide. The neuroprotective effects of propofol against IBI have been previously demonstrated. However, the neuroprotective effects of propofol on hippocampal neurons are not yet entirely clear. In the present study, models of IBI were established in hypoxia-exposed hippocampal neuronal cells. Cell viability assay and apoptosis assay were performed to examine the neuroprotective effects of propofol on hippocampal neurons in IBI. A significant decrease in cell viability and a significant increase in cel...
Source: International Journal of Molecular Medicine - July 4, 2016 Category: Molecular Biology Authors: Gong HY, Zheng F, Zhang C, Chen XY, Liu JJ, Yue XQ Tags: Int J Mol Med 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

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