Protective role of silent information regulator 1 against hepatic ischemia: effects on oxidative stress injury, inflammatory response, and MAPKs

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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Rhubarb-Aconite Decoction (RAD) Drug-Containing Serum Alleviated Endotoxin-Induced Oxidative Stress Injury and Inflammatory Response in Caco-2 Cells In Vitro

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2020/5834502 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Xiao-hong Du ◽

Qing-jun Chen ◽

Jian-bo Song ◽

Yan Xie ◽

Yan Zhi ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Calcium Ion ◽

Lipid Peroxide ◽

Intestinal Injury ◽

Intracellular Free Calcium ◽

Free Calcium ◽

Stress Injury ◽

Oxidative Stress Injury

Rhubarb-Aconite Decoction (RAD), a famous Chinese medicine prescription, has been widely used for treating intestinal injury. However, the effect of RAD on intestinal epithelial cells is unclear. The aim of this study was to investigate the effects of RAD drug-containing serum on the oxidative stress injury and inflammatory response induced by endotoxin (ET) in Caco-2 cells in vitro. Lipid peroxide malondialdehyde (MDA), lactate dehydrogenase (LDH), caspase-11, tumor necrosis factor-α(TNF-α), interleukin-3(IL-3), and cytokeratin (CK)18, adenosine triphosphate (ATP) activity, and intracellular free calcium ion levels were measured. The results showed that ET triggered the activation of caspase-11 and the massive release of TNF-α, increased the inhibitory rate of cell growth, MDA, and LDH expressions in Caco-2 cells. Moreover, RAD drug-containing serum could inhibit caspase-11 activation, decrease the release of TNF-α and IL-3, reduce intracellular free calcium ion, and enhance CK 18 expression and ATP activity. These novel findings demonstrated that ET-induced oxidative stress injury and inflammatory response of Caco-2 cells were improved by RAD drug-containing serum, indicating that RAD may be a good choice for the treatment of intestinal injury.

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Protective role of microRNA-9-5p in oxygen glucose deprivation/reperfusion-induced injury in liver sinusoidal endothelial cell

10.21203/rs.3.rs-19922/v1 ◽

2020 ◽

Author(s):

Yi Duan ◽

Zhifeng Gao ◽

Xiaoyu Wang ◽

Yuanyuan Meng ◽

Huan Zhang

Keyword(s):

Inflammatory Response ◽

Ischemia Reperfusion ◽

Critical Role ◽

Glucose Deprivation ◽

Protective Role ◽

Liver Sinusoidal Endothelial Cell ◽

Liver Sinusoidal Endothelial Cells ◽

Hepatic Ischemia

Abstract Background: Maintenance of the function and survival of liver sinusoidal endothelial cells (LSECs) play a crucial role in hepatic ischemia/reperfusion (I/R) injury, a major cause of liver impairment during surgical treatment. Emerging evidence indicate a critical role of microRNAs in I/R injury. This study aims to investigate whether miR-9-5p exert a protective effect on LSECs in vitro .Methods: We transfected LSECs with miR-9-5p mimic or mimic NC. LSECs were treated with oxygen and glucose deprivation (OGD, 5% CO2 and 95% N2), followed by glucose-free DMEM medium for 6 h, and high-glucose (HG, 30 mmol/L glucose) DMEM medium for 12 h. The biological role of miR-9-5p in I/R-induced LSEC injury was determined. Results: In the in vitro model of OGD/HG injury in LSECs, the expression levels of miR-9-5p were significantly downregulated and those of CXC chemokine receptor-4 (CXCR4) upregulated. LSEC I/R injury led to deteriorated cell death, enhanced oxidative stress and excessive inflammatory response. Mechanistically, we showed that miR-9-5p overexpression significantly upregulated both mRNA and protein levels of CXCR4, followed by rescue of LSECs, ameliorated inflammatory response, and deactivation of pro-apoptotic signaling pathways.Conclusion: miR-9-5p promotes LSEC survival and inhibits apoptosis and inflammatory response in LSECs following OGD/HG injury via downregulation of CXCR4.

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Effect of lentivirus-mediated CFTR overexpression on oxidative stress injury and inflammatory response in the lung tissue of COPD mouse model

Bioscience Reports ◽

10.1042/bsr20193667 ◽

2020 ◽

Vol 40 (1) ◽

Cited By ~ 1

Author(s):

Xiaoli Xu ◽

Huimin Huang ◽

Xiangyi Yin ◽

Hongmei Fang ◽

Xiaoyue Shen

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Mouse Model ◽

Signaling Pathway ◽

Lung Tissue ◽

Negative Control ◽

Chronic Obstructive ◽

Stress Injury ◽

Obstructive Pulmonary Disease ◽

Oxidative Stress Injury

Abstract We aimed to investigate the regulatory mechanism of lentivirus-mediated overexpression of cystic fibrosis transmembrane conductance regulator (CFTR) in oxidative stress injury and inflammatory response in the lung tissue of mouse model of chronic obstructive pulmonary disease (COPD). COPD mouse model induced by cigarette smoke was established and normal mice were used as control. The mice were assigned into a normal group (control), a model group (untreated), an oe-CFTR group (injection of lentivirus overexpressing CFTR), and an oe-NC group (negative control, injection of lentivirus expressing irrelevant sequences). Compared with the oe-NC group, the oe-CFTR group had higher CFTR expression and a better recovery of pulmonary function. CFTR overexpression could inhibit the pulmonary endothelial cell apoptosis, reduce the levels of glutathione (GSH), reactive oxygen species (ROS), and malondialdehyde (MDA) and increase the values of superoxide dismutase (SOD), GSH peroxidase (GSH-Px), and total antioxidant capacity (T-AOC). The overexpression also led to reductions in the white blood cell (WBC) count in alveolus pulmonis, the concentrations of C-reactive protein (CRP), interleukin (IL)-6, and tumor necrosis factor-α, and the protein expressions of NF-κB p65, ERK, JNK, p-EPK, and p-JNK related to MAPK/NF-κB p65 signaling pathway. In conclusion, CFTR overexpression can protect lung tissues from injuries caused by oxidative stress and inflammatory response in COPD mouse model. The mechanism behind this may be related to the suppression of MAPK/NF-κB p65 signaling pathway.

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Oxidative stress induced by tBHP in human normal colon cells by label free Raman spectroscopy and imaging: The protective role of natural antioxidants in the form of β-carotene

10.1101/2021.02.16.431391 ◽

2021 ◽

Author(s):

B. Brozek-Pluska ◽

K. Beton

Keyword(s):

Oxidative Stress ◽

Human Colon ◽

Protective Role ◽

Control Group ◽

Label Free ◽

Normal Colon ◽

Stress Injury ◽

Colon Cells ◽

Β Carotene

AbstractThe present study aimed to investigate the protective effect of β-carotene on the oxidative stress injury of human normal colon cell line CCD-18Co triggered by tert-Butyl hydroperoxide (tBHP). XTT examination was used to determine cell viability after β-carotene supplementation and to determine the optimal concentration of antioxidant in spectroscopic studies. Cell biochemistry for CCD-18Co control group, after tBHP adding and for cells in β-carotene - tBHP model was studied by using label-free Raman microspectroscopy. Results for stress treated CCD-18Co human colon normal cells and human colon cancer cells Caco-2 based on vibration features were also compared. Pretreatment with β-carotene alleviated damages in CCD-18Co human normal colon cells induced by tBHP and showed the preventative effect on cells apoptosis. Treatment with β-carotene altered the level of ROS investigated based on intensities of Raman peaks typical for lipids, proteins and nucleic acids. Presented study confirmed the antioxidant, protective role of β-carotene against ROS by using spectroscopic label-free Raman techniques.

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FoxO3 transcription factor promotes autophagy after oxidative stress injury in HT22 cells

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2020-0448 ◽

2020 ◽

Author(s):

Aiqing Deng ◽

Limin Ma ◽

Xueli Zhou ◽

Xin Wang ◽

Shouyan Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Transcription Factors ◽

Cell Injury ◽

Cell Damage ◽

Critical Role ◽

Neuronal Cell ◽

Ht22 Cells ◽

Stress Injury ◽

Oxidative Stress Injury

Autophagy has been implicated in neurodegenerative diseases. Forkhead box O3 (FoxO3) transcription factors promote autophagy in heart and inhibit oxidative damage. Here we investigate the role of FoxO3 transcription factors in regulating autophagy after oxidative stress injury in immortalized mouse hippocampal cell line (HT22). The present study confirms that hydrogen peroxide (H2O2) injury could induce autophagy and FoxO3 activation in HT22 cells. In addition, overexpression of FoxO3 enhanced H2O2-induced autophagy activation and suppressed neuronal cell damage, while knockdown of FoxO3 reduced H2O2-induced autophagy activation and exacerbated neuronal cell injury. Inhibition of autophagy by 3-Methyladenine (3-MA) resulted in reduced cell viability, increased production of reactive oxygen species (ROS), promoted nuclear condensation and decreased expression of antiapoptotic and autophagy-related proteins, indicating that autophagy may have protective effects on H2O2-induced injury in HT22 cells. Moreover, overexpression of FoxO3 prevented exacerbation of brain damage induced by 3-MA. Taken together, these results show that activation of FoxO3 could induce autophagy and inhibit H2O2-induced damage in HT22 cells. Our study demonstrates the critical role of FoxO3 in regulating autophagy in brain.

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