Olive-Leaf Extracts Modulate Inflammation and Oxidative Stress Associated with Human H. pylori Infection

Helicobacter pylori (H. pylori) is one of the major human pathogens and the main cause of pathological damages that can progress from chronic gastritis to gastric cancer. During the colonization of gastric mucosa, this bacterium provokes a strong inflammatory response and subsequent oxidative process, which are associated with tissue damage. Therefore, the objective of this research was to evaluate the ability of two olive-leaf extracts (E1 and E2) to modulate the inflammatory response and oxidative stress in H. pylori-infected human gastric AGS cells. The obtained results showed that both extracts significantly decreased interleukin-8 (IL-8) secretion and reactive oxygen species (ROS) production in human gastric AGS cells. Both extracts also showed antibacterial activity against different H. pylori strains. HPLC-PAD-MS characterization demonstrated that extract E1 was mainly composed of highly hydrophilic compounds, such as hydroxytyrosol (HT) and its glucosides, and it was the most effective extract as an antibacterial agent. In contrast, extract E2 was composed mostly of moderately hydrophilic compounds, such as oleuropein (OLE), and it was more effective than extract E1 as an anti-inflammatory agent. Both extracts exhibited similar potential to decrease ROS production. These results show the importance of standardizing the extract composition according to the bioactive properties that should be potentiated.

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Screening and Estimation of Secondary Metabolites in Leaf Extracts of Delonix elata (L.) Gamble and their Inhibitory Activities against Pathogens and Oxidative Stress

International Journal of Pharmaceutical Sciences and Nanotechnology ◽

10.37285/ijpsn.2020.13.3.5 ◽

2020 ◽

Vol 13 (3) ◽

pp. 4918-4925

Author(s):

M Mala ◽

◽

G Jeya Jothi

Keyword(s):

Oxidative Stress ◽

Secondary Metabolites ◽

Leaf Extracts ◽

Inhibitory Activities ◽

And Oxidative Stress

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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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Cudrania tricuspidata Root Extract Prevents Methylglyoxal-Induced Inflammation and Oxidative Stress via Regulation of the PKC-NOX4 Pathway in Human Kidney Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/5511881 ◽

2021 ◽

Vol 2021 ◽

pp. 1-13

Author(s):

Donghee Kim ◽

Jayeon Cheon ◽

Haelim Yoon ◽

Hee-Sook Jun

Keyword(s):

Oxidative Stress ◽

Protein Kinase ◽

Antioxidant Enzyme ◽

Root Extract ◽

Kidney Cells ◽

Nuclear Factor ◽

Ros Production ◽

Cudrania Tricuspidata ◽

Pkc Activation ◽

And Oxidative Stress

Diabetic nephropathy is a microvascular complication induced by diabetes, and methylglyoxal (MGO) is a reactive carbonyl species causing oxidative stress that contributes to the induction of inflammatory response in kidney cells. Cudrania tricuspidata (CT), cultivated in Northeast Asia, has been used as traditional medicine for treating various diseases, including neuritis, liver damage, and cancer. In this study, we determined whether a CT root extract (CTRE) can prevent MGO-induced reactive oxygen species (ROS) production and inflammation and assessed underlying mechanisms using a kidney epithelial cell line, HK-2. We observed that CTRE inhibited MGO-induced ROS production. Additionally, CTRE ameliorated the activation of MGO-induced inflammatory signaling pathways such as p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), and c-JUN N-terminal kinase (JNK). Consistent with these results, expressions of p-nuclear factor-kappa B (NFκB) and inflammatory cytokines, tumor necrosis factor-α, interleukin- (IL-) 1β, and IL-6, were decreased when compared with MGO-only exposed HK-2 cells. CTRE alleviated the MGO-induced decrease in nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and antioxidant enzyme mRNA expressions. MGO induced the expression of NADPH oxidase 4 (NOX4); CTRE pretreatment inhibited this induction. Further studies revealed that the NOX4 expression was inhibited owing to the suppression of MGO-induced protein kinase C (PKC) activation following CTRE treatment. Collectively, our data suggest that CTRE attenuates MGO-induced inflammation and oxidative stress via inhibition of PKC activation and NOX4 expression, as well as upregulating the Nrf2-antioxidant enzyme pathway in HK-2 cells.

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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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