Quercetin in attenuation of ischemic/reperfusion injury: A review

2020 ◽  
Vol 13 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Saeed Samarghandian ◽  
Kiavash Hushmandi ◽  
Amirhossein Zabolian ◽  
Md Shahinozzaman ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Membrane ◽  
Blood Supply ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Membrane Integrity ◽  
Therapeutic Effects ◽  
Molecular Pathways ◽  
Cell Membrane Integrity ◽  
Cell Membrane Disruption

Background: Ischemia/reperfusion (I/R) injury is a serious pathologic event that occurs due to restriction in blood supply to an organ, followed by hypoxia. This condition leads to enhanced levels of pro-inflammatory cytokines such as IL-6 and TNF-, and stimulation of oxidative stress via enhancing reactive oxygen species (ROS) levels. Upon reperfusion, blood supply increases, but it deteriorates condition, and leads to generation of ROS, cell membrane disruption and finally, cell death. Plant derived-natural compounds are well-known due to their excellent antioxidant and anti-inflammatory activities. Quercetin is a flavonoid exclusively found in different vegetables, herbs, and fruits. This naturally occurring compound possesses different pharmacological activities making it appropriate option in disease therapy. Quercetin can also demonstrate therapeutic effects via affecting molecular pathways such as NF-B, PI3K/Akt and so on. Methods: In the present review, we demonstrate that quercetin administration is beneficial in ameliorating I/R injury via reducing ROS levels, inhibition of inflammation, and affecting molecular pathways such as TLR4/NF-B, MAPK and so on. Results and conclusion: Quercetin can improve cell membrane integrity via decreasing lipid peroxidation. Apoptotic cell death is inhibited by quercetin via down-regulation of Bax, and caspases, and upregulation of Bcl-2. Quercetin is able to modulate autophagy (inhibition/induction) in decreasing I/R injury. Nanoparticles have been applied for delivery of quercetin, enhancing its bioavailability and efficacy in alleviation of I/R injury. Noteworthy, clinical trials have also confirmed the capability of quercetin in reducing I/R injury.

Adaptive Responses to the Stress Induced by Hyperthermia or Hydrogen Peroxide in Human Fibroblasts

2003 ◽  
Vol 228 (5) ◽  
pp. 491-498 ◽  
Author(s):  
S. Grasso ◽  
C. Scifo ◽  
V. Cardile ◽  
R. Gulino ◽  
M. Renis
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Ischemia Reperfusion Injury ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Human Fibroblasts ◽  
Membrane Integrity ◽  
Adaptive Responses ◽  
Mitochondrial Potential ◽  
Cell Membrane Integrity

Perturbation of oxidant/antioxidant cellular balance, induced by cellular metabolism and by exogenous sources, causes deleterious effects to proteins, lipids, and nucleic acids, leading to a condition named “oxidative stress” that is involved in several diseases, such as cancer, ischemia-reperfusion injury, and neurodegenerative disorders. Among the exogenous agents, both H2O2 and hyperthermia have been implicated in oxidative stress promotion linked with the activation of apoptotic or necrotic mechanisms of cell death. The goal of this work was to better understand the involvement of some stress-related proteins in adaptive responses mounted by human fibroblasts versus the oxidative stress differently induced by 42°C hyperthermia or H2O2. The research was developed, switching off inducible nitric oxide synthase (iNOS) expression through antisense oligonucleotide transfection by studying the possible coregulation in the expression of HSP32 (also named HO-1), HSP70, and iNOS and their involvement in the induction of DNA damage. Several biochemical parameters, such as cell viability (MTT assay), cell membrane integrity (lactate dehydrogenase release), reactive oxygen species formation, glutathione levels, immunocytochemistry analysis of iNOS, HSP70, and HO-1 levels, genomic DNA fragmentation (HALO/COMET assay), and transmembrane mitochondrial potential (ΔΨ) were examined. Cells were collected immediately at the end of the stress-inducing treatment. The results, confirming the pleiotropic function of i-NOS, indicate that: (i) HO-1/HSP32, HSP70, and iNOS are finely tuned in their expression to contribute all together, in human fibroblasts, in ameliorating the resistance to oxidative stress damage; (ii) ROS exposure, at least in hyperthermia, in human fibroblasts contributes to growth arrest more than to apoptosis activation; and (iii) mitochondrial dysfunction, in presence of iNOS inhibition seems to be clearly involved in apoptotic cell death of human fibroblasts after H2O2 treatment, but not after hyperthermia.

scholarly journals Pyrrolidine dithiocarbamate restores endothelial cell membrane integrity and attenuates monocrotaline-induced pulmonary artery hypertension

2008 ◽  
Vol 294 (6) ◽  
pp. L1250-L1259 ◽  
Author(s):  
Jing Huang ◽  
Pawel M. Kaminski ◽  
John G. Edwards ◽  
Albert Yeh ◽  
Michael S. Wolin ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Membrane ◽  
Pulmonary Artery ◽  
Membrane Integrity ◽  
Pulmonary Artery Hypertension ◽  
Pyrrolidine Dithiocarbamate ◽  
Cell Membrane Integrity ◽  
Protein Activation ◽  
Caveolin 1 ◽  
Cell Membrane Disruption

Monocrotaline (MCT)-induced pulmonary artery hypertension (PAH) in rats is preceded by an inflammatory response, progressive endothelial cell membrane disruption, reduction in the expression of caveolin-1, and reciprocal activation of STAT3 (PY-STAT3). Superoxide and NF-κB have been implicated in PAH. To evaluate the role of caveolin-1, PY-STAT3 activation, and superoxide in PAH, MCT-injected rats were treated daily with pyrrolidine dithiocarbamate (PDTC; starting on days 1, 3, and 14 × 2 wk), an inhibitor of inflammation and NF-κB activation. Hemodynamic data, the expression of inhibitory (I)-κBα, caveolin-1, and Tie2 (a membrane protein), activation of PY-STAT3 and NF-κB, and superoxide chemiluminescence were examined. Rats developed progressive PAH at 2 wk post-MCT. There was progressive reduction in the expression of caveolin-1, Tie2, and activation of PY-STAT3 in the lungs. Reduction in I-κBα expression was present at 2 and 4 wk post-MCT. Superoxide chemiluminescence and NF-κB activation were observed only at 2 wk post-MCT and both decreased by 4 wk post-MCT despite progressive PAH. PDTC (starting on days 1 and 3) rescued caveolin-1 and Tie2, reversed MCT-induced PY-STAT3 activation, and attenuated PAH. In addition, PDTC restored I-κBα expression and reduced superoxide chemiluminescence at 2 wk but did not inhibit NF-κB activation despite attenuation of PAH. PDTC had no effect on established PAH. Increased superoxide chemiluminescence and NF-κB activation appear to be a transient phenomenon in the MCT model. Thus the disruption of endothelial cell membrane integrity resulting in caveolin-1 loss and reciprocal activation of PY-STAT3 plays a key role in the MCT-induced PAH.

Determining the fate of Microcystis aeruginosa cells and microcystin toxins following chloramination

2010 ◽  
Vol 62 (2) ◽  
pp. 442-450 ◽  
Author(s):  
Lionel Ho ◽  
Nawal Kayal ◽  
Rino Trolio ◽  
Gayle Newcombe
Keyword(s):  
Cell Membrane ◽  
Microcystis Aeruginosa ◽  
Flow Cytometric Analysis ◽  
Membrane Integrity ◽  
Water Source ◽  
High Dose ◽  
Drinking Water Source ◽  
Pseudo First Order Reaction ◽  
Cell Membrane Integrity ◽  
Cell Membrane Disruption

The cyanobacterium Microcystis aeruginosa can produce potent toxins known as microcystins. While many studies have focussed on the chlorination of microcystin toxins, little work has been conducted with respect to the chloramination of the microcystins. In addition, no studies have been reported on the effect of chloramination on intact Microcystis cells. This study was conducted to determine the fate of M. aeruginosa cells and microcystin toxins following chloramination of a drinking water source. Results indicate that monochloramine could effectively oxidise dissolved microcystin-LR (MCLR) provided high CT values were employed, typically greater than 30,000 mg min L−1. The decay of MCLR was demonstrated to be a pseudo first-order reaction with rate constants ranging from 9.3 × 10−7 to 1.1 × 10−5 s−1 at pH 8.5. However, in the presence of Microcystis cells, monochloramine was ineffective in oxidising microcystin toxins due to the cells exerting a demand on the oxidant. The doses of monochloramine applied (2.8 and 3.5 mg L−1) were shown to rapidly release intracellular microcystins into the dissolved state. Flow cytometric analysis of the cells determined that the lower monochloramine dose did not compromise the cell membrane integrity, even though microcystins were rapidly released from the cells. In contrast the higher monochloramine dose resulted in cell membrane disruption with up to 90% of the cells shown to be non-viable after the high dose was applied.

scholarly journals The Drosophila TNF Eiger activates caspase-dependent necrosis when apoptosis is blocked

2018 ◽  
Author(s):  
Mingli Li ◽  
Yun Fan
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Membrane Integrity ◽  
Apoptotic Cell Death ◽  
Dual Roles ◽  
Developmental Defects ◽  
Cell Membrane Integrity ◽  
Effector Caspases ◽  
Necrosis Factor ◽  
Cellular Organelles

AbstractEiger (Egr), the homolog of the mammalian tumor-necrosis factor (TNF), is the ligand of the c-Jun N-terminal kinase (JNK) stress response signaling pathway in Drosophila. Although expression of Egr frequently leads to apoptosis, it has also been implicated in activation of non-apoptotic cell death. However, it is not yet clear how Egr can induce both apoptosis and non-apoptotic cell death, and if so, how such processes are coordinated. Here, we show that expression of Egr in the developing Drosophila eye induces apoptosis and non-apoptotic developmental defects, both of which are JNK-dependent. Intriguingly, when apoptotic effector caspases DrICE and Dcp-1 are defective or inhibited, expression of Egr induces necrosis characterized by loss of cell membrane integrity, translucent cytoplasm and aggregation of cellular organelles. Surprisingly, the induction of necrosis depends on the catalytic activity of the initiator caspase Dronc and the input from JNK signaling independently of their roles in apoptosis. Therefore, similar to the mammalian caspase-8, caspases in Drosophila also have dual roles in promoting TNF-mediated apoptosis and inhibiting necrosis.

scholarly journals Gasdermins: pore-forming activities and beyond

2020 ◽  
Vol 52 (5) ◽  
pp. 467-474
Author(s):  
Zengzhang Zheng ◽  
Wanyan Deng ◽  
Xiwen Lou ◽  
Yang Bai ◽  
Junhong Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Membrane ◽  
Domain Structure ◽  
Expression Profile ◽  
Inflammatory Mediators ◽  
Inflammatory Cell ◽  
Current Knowledge ◽  
Membrane Integrity ◽  
Spontaneous Mutations ◽  
Cell Membrane Integrity

Abstract Gasdermins (GSDMs) belong to a protein superfamily that is found only in vertebrates and consists of GSDMA, GSDMB, GSDMC, GSDMD, DFNA5 (a.k.a. GSDME) and DFNB59 (a.k.a. Pejvakin (PJVK)) in humans. Except for DFNB59, all members of the GSDM superfamily contain a conserved two-domain structure (N-terminal and C-terminal domains) and share an autoinhibitory mechanism. When the N-terminal domain of these GSDMs is released, it possesses pore-forming activity that causes inflammatory death associated with the loss of cell membrane integrity and release of inflammatory mediators. It has also been found that spontaneous mutations occurring in the genes of GSDMs have been associated with the development of certain autoimmune disorders, as well as cancers. Here, we review the current knowledge of the expression profile and regulation of GSDMs and the important roles of this protein family in inflammatory cell death, tumorigenesis and other related diseases.

scholarly journals Poloxamer 188 Attenuates Ischemia-Reperfusion-Induced Lung Injury by Maintaining Cell Membrane Integrity and Inhibiting Multiple Signaling Pathways

2021 ◽  
Vol 12 ◽  
Author(s):  
Shih-En Tang ◽  
Wen-I Liao ◽  
Hsin-Ping Pao ◽  
Chin-Wang Hsu ◽  
Shu-Yu Wu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cells ◽  
Cell Membrane ◽  
Lung Injury ◽  
Signaling Pathways ◽  
Ischemia Reperfusion ◽  
Membrane Integrity ◽  
Poloxamer 188 ◽  
Cell Membrane Integrity ◽  
Multiple Signaling

Background: Poloxamer 188 (P188) possesses anti-inflammatory properties and can help to maintain plasma membrane function. P188 has been reported to exert beneficial effects in the treatment of various disorders. However, the effects of P188 in ischemia/reperfusion (IR)-induced acute lung injury have not been examined.Methods: We investigated the ability of P188 to attenuate IR-induced acute lung injury in rats and hypoxia/reoxygenation (HR) injury in murine epithelial cells. Isolated perfused rat lungs were exposed to 40 min ischemia followed by 60 min reperfusion to induce IR injury.Results: IR led to lung edema, increased pulmonary arterial pressure, promoted lung tissue inflammation and oxidative stress, and upregulated the levels of TNF-α, IL-6 and CINC-1, and increased Lactic dehydrogenase (LDH) activity in bronchoalveolar lavage fluid. IR also downregulated the levels of inhibitor of κB (IκB-α), upregulated nuclear factor (NF)-κB (NF-κB), and promoted apoptosis in lung tissues. P188 significantly suppressed all these effects. In vitro, P188 also exerted a similar effect in murine lung epithelial cells exposed to HR. Furthermore, P188 reduced the number of propidium iodide-positive cells, maintained cell membrane integrity, and enhanced cell membrane repair following HR.Conclusion: We conclude that P188 protects against lung IR injury by suppressing multiple signaling pathways and maintaining cell membrane integrity.

scholarly journals Shell thickness-dependent antibacterial activity and biocompatibility of gold@silver core–shell nanoparticles

RSC Advances ◽  
2017 ◽  
Vol 7 (19) ◽  
pp. 11355-11361 ◽  
Author(s):  
Longping Yang ◽  
Wenjing Yan ◽  
Hongxia Wang ◽  
Hong Zhuang ◽  
Jianhao Zhang
Keyword(s):  
Antibacterial Activity ◽  
Cell Membrane ◽  
Membrane Integrity ◽  
Membrane Disruption ◽  
Ag Nps ◽  
Shell Nanoparticles ◽  
Cell Membrane Integrity ◽  
Gold Silver ◽  
Cell Membrane Disruption ◽  
Core Shell Nanoparticles

The Au@Ag NPs exhibit synergistically enhanced antibacterial activity and kill bacteria by affecting the cell membrane integrity or causing cell membrane disruption.

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