Lysergic acid diethylamide causes photoreceptor cell damage through inducing inflammatory response and oxidative stress

Abstract Lysergic acid diethylamide (LSD) is a classic hallucinogen, widely abused for decades, while phencyclidine (PCP) has increased in popularity in recent years, especially among the adolescents. Very little is known about the general toxicity of these compounds, especially about their possible neurotoxic effects at the cell level. The aim of this study was to address these gaps by assessing the toxic effects of 24-hour exposure to LSD and PCP in the concentration range of 0.39–100 μmol/L in the human neuroblastoma SH-SY5Y cell line. After cell viability was established, cells treated with concentrations that reduced their viability up to 30 % were further subjected to the alkaline comet assay and biochemical assays that enable estimation of oxidative stress-related effects. Treatment with LSD at 6.25 μmol/L and with PCP at 3.13 μmol/L resulted with 88.06±2.05 and 84.17±3.19 % of viable cells, respectively, and led to a significant increase in primary DNA damage compared to negative control. LSD also caused a significant increase in malondialdehyde level, reactive oxygen species (ROS) production, and glutathione (GSH) level, PCP significantly increased ROS but lowered GSH compared to control. Treatment with LSD significantly increased the activities of all antioxidant enzymes, while PCP treatment significantly increased superoxide dismutase (SOD) and glutathione peroxidase (GPx) but decreased catalase (CAT) activity compared to control. Our findings suggest that LSD has a greater DNA damaging potential and stronger oxidative activity than PCP in SH-SY5Y cells.

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UFL1 Alleviates Lipopolysaccharide-Induced Cell Damage and Inflammation via Regulation of the TLR4/NF-κB Pathway in Bovine Mammary Epithelial Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/6505373 ◽

2019 ◽

Vol 2019 ◽

pp. 1-17 ◽

Cited By ~ 6

Author(s):

Chengmin Li ◽

Lian Li ◽

Kunlin Chen ◽

Yiru Wang ◽

Fangxiao Yang ◽

...

Keyword(s):

Oxidative Stress ◽

Epithelial Cells ◽

Inflammatory Response ◽

Er Stress ◽

Mammary Epithelial Cells ◽

Cell Damage ◽

Mammary Epithelial ◽

Cellular Stress Response ◽

Bovine Mammary Epithelial Cells ◽

And Oxidative Stress

In recent studies, UFL1 (ubiquitin-like modifier 1 ligating enzyme 1) has been identified as a significant regulator of NF-κB signaling and cellular stress response, yet its physiological function in LPS-stimulated bovine mammary epithelial cells (BMECs) remains unknown. In this study, we investigated the modulating effect of UFL1 on the regulation of LPS-induced inflammation and cell damage, with a focus on apoptosis, ER stress, autophagy, oxidative stress, and the TLR4/NF-κB signaling pathway. The results showed that UFL1 depletion aggravated the LPS-induced inflammatory response and cell damage by positively regulating the TLR4/NF-κB pathway (increased the expression of TLR4, NF-κB P65 in nuclear, and phospho-IκBα), exacerbating LPS-induced ER stress (increased the expression of CHOP, Hsp70, and GRP78), apoptosis (increased the expression of Bax/Bcl-2 and activity of caspase-3), autophagy (increased LC3-II and decreased P62 expression), and oxidative stress (decreased SOD and CAT levels and increased MDA levels). Overexpression of UFL1 suppressed the activation of the TLR4/NF-κB pathway and relieved the LPS-induced ER stress, apoptosis, autophagy, and oxidative stress, thereby alleviating the inflammatory response and cell damage. Collectively, UFL1 may play an important role during the inflammatory response and thereby acts as a potential therapeutic target for bovine mastitis.

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miR-124-3p targeted SIRT1 to regulate cell apoptosis, inflammatory response, and oxidative stress in acute myocardial infarction in rats via modulation of the FGF21/CREB/PGC1α pathway

Journal of Physiology and Biochemistry ◽

10.1007/s13105-021-00822-z ◽

2021 ◽

Author(s):

Yun-Jie Wei ◽

Jun-Feng Wang ◽

Fei Cheng ◽

Hai-Jun Xu ◽

Jia-Juan Chen ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Inflammatory Response ◽

Cell Apoptosis ◽

And Oxidative Stress

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Dexmedetomidine inhibits inflammatory response and oxidative stress through regulating miR-205-5p by targeting HMGB1 in cerebral ischemic/reperfusion

Immunopharmacology and Immunotoxicology ◽

10.1080/08923973.2021.1942901 ◽

2021 ◽

pp. 1-9

Author(s):

Jun-jun Yang ◽

Yan-Hong Zhao ◽

Ke-Wen Yin ◽

Xiao-qing Zhang ◽

Jianhui Liu

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Ischemic Reperfusion ◽

Cerebral Ischemic ◽

Cerebral Ischemic Reperfusion ◽

And Oxidative Stress

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Cyane-carvone, a Synthetic Derivative of Carvone, Inhibits Inflammatory Response by Reducing Cytokine Production and Oxidative Stress and Shows Antinociceptive Effect in Mice

Inflammation ◽

10.1007/s10753-014-9817-1 ◽

2014 ◽

Author(s):

Thiago Henrique Costa Marques ◽

Maria Leonildes Boavista Gomes Cast Marques ◽

Jand-Venes R. Medeiros ◽

Renan Oliveira Silva ◽

André Luiz dos Reis Barbosa ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Cytokine Production ◽

Antinociceptive Effect ◽

Synthetic Derivative ◽

And Oxidative Stress

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Simultaneous miRNA and mRNA Transcriptome Profiling of Differentiating Equine Satellite Cells Treated with Gamma-Oryzanol and Exposed to Hydrogen Peroxide

Nutrients ◽

10.3390/nu10121871 ◽

2018 ◽

Vol 10 (12) ◽

pp. 1871

Author(s):

Karolina Chodkowska ◽

Anna Ciecierska ◽

Kinga Majchrzak ◽

Piotr Ostaszewski ◽

Tomasz Sadkowski

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Hydrogen Peroxide ◽

Cell Viability ◽

Satellite Cells ◽

Cell Damage ◽

Quantitative Polymerase Chain Reaction ◽

Mirna Gene ◽

Gamma Oryzanol ◽

And Oxidative Stress

Gamma-oryzanol (GO) is a popular supplement for performance horses, dogs, and humans. Previous studies indicated that GO supplementation decreases creatine kinase activity and lactate level after exercise and may affect oxidative stress in Thoroughbred horses. GO may change genes expression in equine satellite cells (ESC). The purpose of this study was to evaluate the effect of GO on miRNA, gene expression, oxidative stress, and cell damage and viability in differentiating ESC pretreated with hydrogen peroxide (H2O2). ESCs were obtained from a young horse’s skeletal muscle. ESCs were pre-incubated with GO (24 h) and then exposed to H2O2 for one hour. For the microRNA and gene expression assessment, the microarray technique was used. Identified miRNAs and genes were validated using real time-quantitative polymerase chain reaction. Several tests related to cell viability, cell damage, and oxidative stress were performed. The microarray analysis revealed differences in 17 miRNAs and 202 genes between GO-treated and control ESC. The tests related to apoptosis, cell viability, and oxidative stress showed that GO affects these processes to varying degrees. Our results suggest that GO can change miRNA and gene expression and may impact the processes involved in tissue repairing after an injury.

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Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

Journal of Immunology Research ◽

10.1155/2021/2389029 ◽

2021 ◽

Vol 2021 ◽

pp. 1-10

Author(s):

Haijun Zhao ◽

Yanhui He

Keyword(s):

Oxidative Stress ◽

Stem Cells ◽

Bone Marrow ◽

Endothelial Cells ◽

Inflammatory Response ◽

Protective Effects ◽

Stress Injury ◽

Oxidative Stress Injury ◽

Marrow Mesenchymal Stem Cells ◽

And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

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