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Aim To investigate the protective effect of essential oil from Fructus Alpiniae Zerumbet (EOFAZ ) on type 2 diabetes-induced pancreatic injury in mice and its mechanism.Methods After C57 BL/6 mice fed with high-sugar and high-fat ( HFS) feed developed insulin resistance, streptozotocin ( STZ, 120 mg • kg 1 ) was injected intraperitoneal
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Aim To investigate the protective effect of cardiopulmonary resuscitation (CPR) on hippocampal brain tissues of rats after cardiac arrest and its mechanism. Methods Forty SD rats were randomly divided into control group, ischemia group, cardiopulmonary resuscitation group and Edaravone treatment group. The rats in ischemia group were subjected to cardiac arrest by suffocation for 10 min. In resuscitation group, cardiac arrest/cardiopulmonary resuscitation (CA/CPR) was performed, after 3 min of cardiac arrest, cardiopulmonary resuscitation was performed for 7 min. After 10 min, the rats in each group were sacrificed, venous blood was taken to detect oxidative stress indicators, and the pathology of rat hippocampal brain tissues were examined by HE staining and electron microscopy, and the expressions of Nrf2 and Keapl gene and proteins were detected by real-time fluorescent quantitative PCR and Western blot. Results Compared with control group, the serum oxidative stress level of the ischemic model group rats increased, the Nissl body of the hippocampal nerve cells decreased significantly, the mitochondrial cristae were destroyed significantly, and the expressions of Nrf2 and Keapl genes and proteins in the hippocampal tissues increased. Compared with ischemic group, the serum oxidative stress level of resuscitation group rats decreased. Compared with ischemic group, the serum oxidative stress level of the rats in cardiopulmonary resuscitation group decreased, the neuronal cells in the hippocampus increased, the mitochondrial cristae damage was alleviated, and the expressions of Nrf2 and Keapl genes and proteins in the hippocampus decreased. Conclusions CPR has protective effect on hippocampal tissues of rats, and its mechanism is related to the alleviation of Nrf2/Keapl pathway of oxidative stress injury.
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Keapl-Nrf2-ARE pathway represents one of the most important cellular defense mechanisms against oxidative stress. The expression of various detoxifying, antioxidant defense enzymes and proteins depend on the activation of the Nr£2 signaling. Keapl-Nrf2-ARE signaling pathway has become an attractive target for the prevention and treatment of oxidative stress-related diseases including neurodegenerative, cancer, cardiovascular, metabolic and inflammatory diseases. Activating Nrf2 signaling pathway can prevent and treat various oxidative stress-induced diseases. Therefore, discovering and studying the activators of Nrf2 has received extensive attention from researchers. In this paper, we have summarized the mechanism of the Keapl-Nrf2-ARE pathway and the research progress of some small molecule activators in this pathway.
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Aim: To study the induction of apoptotic effect of sodium selenite on human lung cancer A549 cells and its mechanisms. Methods: A549 cells were exposed to different concentrations of sodium selenite for 24 h. MTT assay was applied to determine A549 cell proliferation. Inverted fluorescence microscope was used to investigate the morphological changes in A549 cells. Flow cytometry analysis was applied to assess the apoptotic rates of A549 cells. Laser confocal microscope was employed to measure the reactive oxygen species (ROS) fluorescence intensity. A multi-detection reader was used to determine the antioxidant parameter. Western blot was utilized to detect the expression of Keapl, Nrf2, HO-1 and Nrf2 in cytoplasm and nucleus. Results: MTT results showed that sodium selenite inhibited the proliferation of A549 cells in a concentration-dependent manner. After treatment with sodium selenite for 24 h, the apoptotic rate of A549 cells was markedly increased through Hoechst 33342 staining and flow cytometry measurement. Sodium selenite significantly up-regulated ROS and malondialdehyde (MDA) content and down-regulated the levels of superoxide dismutase (SOD) and glutathione (GSH). Meanwhile, sodium selenite treatment also reduced the expressions of Keapl, Nrf2 and HO-1 at protein levels and inhibited Nrf2 protein nuclear translocation in A549 cells. Conclusions: Treatment with sodium selenite induces A549 cells apoptosis, which may contribute to the anti-proliferation activity, induction of apoptosis and regulation of oxidative stress reaction and Keapl/Nrf2/ARE antioxidative signaling pathway expression.
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Liver can regenerate after chemical damage or partial hepatectomy. Liver regeneration is a complex process involving a variety of cytokines und multiple signal pathways. NK2 is a sensitive transcription factor of oxidation-reduction, which plays a regulatory role in cell defense, oxidation-reduction balance, inflammation and intermediate metabolism. It is closely related to cell proliferation. Some reports ha\e proved that liver regeneration is delayed after partial hepalectomy. Furthermore, ihis phenomenon is observed in the mice with absence of Nrf2. There fore. NrQ signaling pathway is involved in the process of liver regeneration. This article reviews the role of Nri2 signaling pathway in the process of liver regeneration according to the existing research results. We have also summarized the drugs that may affect liver regeneration or hepatocyte proliferation, hoping to find more drugs for liver diseases and provide ideas for the mechanism of the drugs.
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NAD(P)H:quinone-oxidoreductase-1 (NQO1) is a cytosolic enzyme that catalyses two- or four-electron reduction of many endogenous and environmental quinones using flavin adenine dinucleotide (FAD) as a cofactor. It is a cytosolic enzyme exists as a homodimer and is biochemically distinguished by its prominent ability to use either NADH or NADPH as reducing cofactors and by its suppression by the anticoagulant dicumarol. This enzyme generally considered as a detoxification enzyme due to of its ability to diminish reactive quinones and quinoneimines to its less reactive and less toxic hydroquinones forms. NQO1 is a substantially inducible enzyme that is controlled by the Nrf2-Keap1/ARE pathway. Evidence for the significance of the antioxidant functions of NQO1 in suppression of oxidative stress is provided by manifestations that induction of NQO1 levels or their reduction are associated with reduced and raised susceptibilities to oxidative stress, respectively. The gene coding for NQO1 has two common polymorphisms at nucleotide position 609(C-T) and 465 (C-T) of the human cDNA. C465T causes reduction in enzyme activity, whereas the C609T results in complete loss of enzymatic activity due to protein instability.In this review, we discuss the protective functions of NQO1 and present its possible transcriptional pathways regulating its induction by Nrf2-Keap1/ARE pathway.