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

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.

Download Full-text

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

Expert Opinion on Therapeutic Targets ◽

10.1517/14728222.2016.1153067 ◽

2016 ◽

Vol 20 (5) ◽

pp. 519-531 ◽

Cited By ~ 5

Author(s):

Yang Yang ◽

Song Zhang ◽

Chongxi Fan ◽

Wei Yi ◽

Shuai Jiang ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Protective Role ◽

Hepatic Ischemia ◽

Stress Injury ◽

Oxidative Stress Injury ◽

Silent Information Regulator 1

Download Full-text

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.

Download Full-text

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.

Download Full-text

Protective Effects and Mechanisms of Recombinant Human Glutathione Peroxidase 4 on Isoproterenol-Induced Myocardial Ischemia Injury

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/6632813 ◽

2021 ◽

Vol 2021 ◽

pp. 1-17

Author(s):

Chang Liu ◽

Bozhao Li ◽

Qi Yan ◽

Shaopeng Niu ◽

Yiding Zhao ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Ischemia ◽

Glutathione Peroxidase ◽

In Vitro Model ◽

Cardiomyocyte Apoptosis ◽

Protective Effects ◽

Stress Injury ◽

Oxidative Stress Injury ◽

Vitro Model

Ischemic heart disease (IHD) is a cardiovascular disease with high fatality rate, and its pathogenesis is closely related to oxidative stress. Reactive oxygen species (ROS) in oxidative stress can lead to myocardial ischemia (MI) injury in many ways. Therefore, the application of antioxidants may be an effective way to prevent IHD. In recent years, glutathione peroxidase 4 (GPx4) has received increasing attention due to its antioxidant effect. In a previous study, we used the new chimeric tRNAUTuT6 to express highly active recombinant human GPx4 (rhGPx4) in amber-less Escherichia coli. In this study, we established an isoproterenol- (ISO-) induced MI injury model in rats and an in vitro model to research the protective effect and mechanism of rhGPx4 on MI injury. The results showed that rhGPx4 could reduce the area of myocardial infarction and ameliorate the pathological injury of heart tissue, significantly reduce ISO-induced abnormalities on electrocardiogram (ECG) and cardiac serum biomarkers, protect mitochondrial function, and attenuate cardiac oxidative stress injury. In an in vitro model, the results also confirmed that rhGPx4 could inhibit ISO-induced oxidative stress injury and cardiomyocyte apoptosis. The mechanism of action of rhGPx4 involves not only the inhibition of lipid peroxidation by eliminating ROS but also keeping a normal level of endogenous antioxidant enzymes by eliminating ROS, thereby preventing oxidative stress injury in cardiomyocytes. Additionally, rhGPx4 could inhibit cardiomyocyte apoptosis through a mitochondria-dependent pathway. In short, rhGPx4, a recombinant antioxidant enzyme, can play an important role in the prevention of IHD and may have great potential for application.

Download Full-text

Overexpression of miR-506-3p Aggravates DBP-Induced Testicular Oxidative Stress in Rats by Downregulating ANXA5 via Nrf2/HO-1 Signaling Pathway

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/4640605 ◽

2020 ◽

Vol 2020 ◽

pp. 1-13

Author(s):

Min Tang ◽

Lei Zhang ◽

Zheng Zhu ◽

Ran Li ◽

Shangqian Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Male Rats ◽

Adolescent Male ◽

Seminiferous Tubules ◽

Stress Injury ◽

Oxidative Stress Injury ◽

Testicular Injury

Background. Di-N-butylphthalate (DBP) is a kind of unique endocrine toxicity linked to hormonal disruptions that affects the male reproductive system and has given rise to more and more attention. However, the mechanism of DBP-induced testicular injury remains unclear. Here, the objective of this study was to investigate the potential molecular mechanism of miR-506-3p in DBP-induced rat testicular oxidative stress injury via ANXA5 (Annexin A5)/Nrf2/HO-1 signaling pathway. Methods. In vivo, a total of 40 adolescent male rats were treated from 2 weeks with 800 mg/kg/day of DBP in 1 mL/kg corn oil administered daily by oral gavage. Among them, some rats were also injected subcutaneously with 2 nmol agomir-506-3p and/or 10 nmol recombinant rat ANXA5. The pathomorphological changes of testicular tissue were assessed by histological examination, and the antioxidant factors were evaluated. Subsequently, ANXA5, Nrf2, and its dependent antioxidant enzymes, such as HO-1, NQO1, and GST, were detected by Western blotting or immunohistochemical staining. In vitro, TM3 cells (Leydig cells) were used to detect the cell activity by CCK-8 and the transfection in the DBP-treated group. Results. Differentially expressed miRNAs between the DBP-treated and normal rats were analyzed, and qRT-PCR showed miR-506-3p was highly expressed in testicular tissues of the DBP-treated rats. DBP-treated rats presented severe inflammatory infiltration, increased abnormal germ cells, and missed cell layers frequently existed in seminiferous tubules, resulted in oxidative stress and decreased testicular function. Meanwhile, upregulation of miR-506-3p aggravated the above changes. In addition, miR-506-3p directly bound to ANXA5, and overexpression of miR-506-3p could reduce the ANXA5 expression and also decrease the protein levels of Nrf2/HO-1 signaling pathway. Additionally, we found that recombinant rat ANXA5 reversed the DBP-treated testicular oxidative stress promoting injury of miR-506-3p in rats. In vivo results were reproduced in in vitro experiments. Conclusions. This study provided evidence that miR-506-3p could aggravate the DBP-treated testicular oxidative stress injury in vivo and in vitro by inhibiting ANXA5 expression and downregulating Nrf2/HO-1 signaling pathway, which might provide novel understanding in DBP-induced testicular injury therapy.

Download Full-text

Carbon monoxide inhibits the nuclear-cytoplasmic translocation of HMGB1 in an in vitro oxidative stress injury model of mouse renal tubular epithelial cells

Journal of Huazhong University of Science and Technology [Medical Sciences] ◽

10.1007/s11596-016-1663-y ◽

2016 ◽

Vol 36 (6) ◽

pp. 791-795 ◽

Cited By ~ 4

Author(s):

Yu Jia ◽

Lu Wang ◽

Guang-yuan Zhao ◽

Zhi-qiang Wang ◽

Song Chen ◽

...

Keyword(s):

Oxidative Stress ◽

Carbon Monoxide ◽

Epithelial Cells ◽

Tubular Epithelial Cells ◽

Renal Tubular Epithelial Cells ◽

Stress Injury ◽

Oxidative Stress Injury ◽

Injury Model ◽

Renal Tubular

Download Full-text

In vitro protective effects of encapsulated quercetin in neuronal models of oxidative stress injury

Biotechnology & Biotechnological Equipment ◽

10.1080/13102818.2017.1347523 ◽

2017 ◽

Vol 31 (5) ◽

pp. 1055-1063 ◽

Cited By ~ 6

Author(s):

Denitsa Aluani ◽

Virginia Tzankova ◽

Yordan Yordanov ◽

Magdalena Kondeva-Burdina ◽

Krassimira Yoncheva

Keyword(s):

Oxidative Stress ◽

Protective Effects ◽

Stress Injury ◽

Oxidative Stress Injury

Download Full-text

Ceftriaxone Calcium Crystals Induce Acute Kidney Injury by NLRP3-Mediated Inflammation and Oxidative Stress Injury

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/6428498 ◽

2020 ◽

Vol 2020 ◽

pp. 1-13

Author(s):

Zhang Yifan ◽

Ning Benxiang ◽

Xu Zheng ◽

Xu Luwei ◽

Zhou Liuhua ◽

...

Keyword(s):

Oxidative Stress ◽

Kidney Injury ◽

Oxidative Stress Markers ◽

Stress Injury ◽

Stress Markers ◽

Oxidative Stress Injury ◽

Calcium Crystals ◽

And Oxidative Stress

Objective. To investigate the role of inflammatory reactions and oxidative stress injury in the mechanisms of ceftriaxone calcium crystal-induced acute kidney injury (AKI) both in vivo and in vitro. Methods. Male Sprague Dawley rats were randomly divided into five groups of ten each according to different concentrations of ceftriaxone and calcium. Based on the levels of serum creatinine (Scr) and blood urea nitrogen (BUN), the AKI group was chosen for the subsequent experiments. Kidney histological examination and immunohistochemistry were performed. The expression of NLRP3 and IL-1β protein and the concentrations of oxidative stress markers such as ROS, MDA, and H2O2 in kidney tissues were estimated. In parallel, HK-2 human renal proximal tubule cells were exposed to ceftriaxone calcium crystals. The mRNA expression levels of NLRP3 and IL-1β and the concentrations of oxidative stress markers were evaluated. Finally, cell viability and rat survival were also assessed. Results. The results showed that significantly increased Scr and BUN levels, consistent with morphological changes and kidney stones, were found in the rats that received the highest concentration of ceftriaxone (1000 mg/kg) combined with calcium (800 mg/kg). The activation of the NLRP3 inflammasome axis and the marked elevation of MDA, H2O2, and ROS levels were observed both in vivo and in vitro. High expression of Nrf2, HO-1, and NQO1 was also documented. In addition, cell apoptosis and rat mortality were promoted by ceftriaxone calcium crystals. Conclusions. Notably, we found that ceftriaxone-induced urolithiasis was associated with a high risk of AKI and NLRP3-mediated inflammasome and oxidative stress injury were of major importance in the pathogenesis.

Download Full-text

Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/8768327 ◽

2019 ◽

Vol 2019 ◽

pp. 1-18 ◽

Cited By ~ 5

Author(s):

Jing Zeng ◽

Long Zhu ◽

Jing Liu ◽

Tao Zhu ◽

Zhaohui Xie ◽

...

Keyword(s):

Oxidative Stress ◽

Ischemic Stroke ◽

Cerebral Ischemia ◽

Ischemia Reperfusion ◽

Luciferase Reporter ◽

Neuroprotective Effects ◽

Stress Injury ◽

Oxidative Stress Injury

Previous studies have shown that metformin not only is a hypoglycemic agent but also has neuroprotective effects. However, the mechanism of action of metformin in ischemic stroke is unclear. Oxidative stress is an important factor in the pathogenesis of cerebral ischemia-reperfusion injury. It has been reported that metformin is associated with stroke risk in the clinical population. This study is aimed at investigating the effect and mechanism of metformin in an experimental model of oxidative stress induced by ischemia/reperfusion (I/R) in vivo and oxygen glucose deprivation/reperfusion (OGD/R) in vitro. Metformin (100, 200, and 300 mg/kg) was administered intraperitoneally immediately after induction of cerebral ischemia. The indicators of oxidative stress selected were antioxidant enzyme activities of catalase, malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), and glutathione peroxidation enzyme (GSHPx). First, we demonstrated that metformin can significantly alleviate acute and chronic cerebral I/R injury and it has a strong regulatory effect on stroke-induced oxidative stress. It can reduce the elevated activities of MDA and NO and increase the levels of GSHPx and SOD in the cerebrum of mice and N2a cells exposed to I/R. Furthermore, real-time PCR and western blot were used to detect the expression of long noncoding RNA H19 (lncRNA-H19), microRNA-148a-3p (miR-148a-3p), and Rho-associated protein kinase 2 (Rock2). The direct interaction of lncRNA-H19, miR-148a-3p, and Rock2 was tested using a dual luciferase reporter assay. lncRNA-H19 altered OGD/R-induced oxidative stress by modulating miR-148a-3p to increase Rock2 expression. The expression of lncRNA-H19 and Rock2 could be downregulated with metformin in vivo and in vitro. In conclusion, our study confirmed that metformin exerts neuroprotective effects by regulating ischemic stroke-induced oxidative stress injury via the lncRNA-H19/miR-148a-3p/Rock2 axis. These results provide new evidence that metformin may represent a potential treatment for stroke-related brain injury.

Download Full-text