scholarly journals Four Novel Dammarane-Type Triterpenoids from Pearl Knots of Panax ginseng Meyer cv. Silvatica

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1159 ◽  
Author(s):  
Zeng Qi ◽  
Zhuo Li ◽  
Xuewa Guan ◽  
Cuizhu Wang ◽  
Fang Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Oxidative Damage ◽  
Cigarette Smoke ◽  
Panax Ginseng ◽  
Inflammatory Reaction ◽  
A549 Cells ◽  
Protective Effects

Panax ginseng Meyer cv. Silvatica (PGS), which is also known as “Lin-Xia-Shan-Shen” or “Zi-Hai” in China, is grown in forests and mountains by broadcasting the seeds of ginseng and is harvested at the cultivation age of 15–20 years. In this study, four new dammarane-type triterpenoids, ginsengenin-S1 (1), ginsengenin-S2 (2), ginsenoside-S3 (3), ginsenoside-S4 (4), along with one known compound were isolated from pearl knots of PGS. Ginsengenin-S2 significantly alleviated oxidative damage when A549 cells were exposed to cigarette smoke (CS) extract. In addition, ginsengenin-S2 could inhibit the CS-induced inflammatory reaction in A549 cells. Protective effects of ginsengenin-S2 against CS-mediated oxidative stress and the inflammatory response in A549 cells may involve the Nrf2 and HDAC2 pathways.

scholarly journals Protective Effects of Quercetin on Livers from Mice Exposed to Long-Term Cigarette Smoke

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Pedro A. Machado-Junior ◽  
Natália P. S. Araújo ◽  
Ana B. F. Souza ◽  
Thalles F. Castro ◽  
Michel Oliveira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cigarette Smoke ◽  
Liver Diseases ◽  
Inflammatory Cells ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Protective Effects ◽  
Histopathological Changes

Cigarette smoke is highly toxic, and it can promote increased production of reactive species and inflammatory response and leads to liver diseases. Quercetin is a flavonoid that displays antioxidant and anti-inflammatory activities in liver diseases. This study aimed at evaluating the protective effects of quercetin on livers from mice exposed to long-term cigarette smoke exposure. Male C57BL/6 mice were divided into five groups: control (CG), vehicle (VG), quercetin (QG), cigarette smoke (CSG), quercetin, and cigarette smoke (QCSG). CSG and QCSG were exposed to cigarette smoke for sixty consecutive days; at the end of the exposures, all animals were euthanized. Mice that received quercetin daily and were exposed to cigarette smoke showed a reduced influx of inflammatory cells, oxidative stress, inflammatory reaction, and histopathological changes in the liver, compared to CSG. These results suggest that quercetin may be an effective adjuvant for treating damage to the liver due to cigarette smoke exposure.

scholarly journals Ethanol Extract of Maclura tricuspidata Fruit Protects SH-SY5Y Neuroblastoma Cells against H2O2-Induced Oxidative Damage via Inhibiting MAPK and NF-κB Signaling

2021 ◽  
Vol 22 (13) ◽  
pp. 6946
Author(s):  
Weishun Tian ◽  
Suyoung Heo ◽  
Dae-Woon Kim ◽  
In-Shik Kim ◽  
Dongchoon Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxidative Damage ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Biologically Active ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Neuroprotective Effects

Free radical generation and oxidative stress push forward an immense influence on the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Maclura tricuspidata fruit (MT) contains many biologically active substances, including compounds with antioxidant properties. The current study aimed to investigate the neuroprotective effects of MT fruit on hydrogen peroxide (H2O2)-induced neurotoxicity in SH-SY5Y cells. SH-SY5Y cells were pretreated with MT, and cell damage was induced by H2O2. First, the chemical composition and free radical scavenging properties of MT were analyzed. MT attenuated oxidative stress-induced damage in cells based on the assessment of cell viability. The H2O2-induced toxicity caused by ROS production and lactate dehydrogenase (LDH) release was ameliorated by MT pretreatment. MT also promoted an increase in the expression of genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). MT pretreatment was associated with an increase in the expression of neuronal genes downregulated by H2O2. Mechanistically, MT dramatically suppressed H2O2-induced Bcl-2 downregulation, Bax upregulation, apoptotic factor caspase-3 activation, Mitogen-activated protein kinase (MAPK) (JNK, ERK, and p38), and Nuclear factor-κB (NF-κB) activation, thereby preventing H2O2-induced neurotoxicity. These results indicate that MT has protective effects against H2O2-induced oxidative damage in SH-SY5Y cells and can be used to prevent and protect against neurodegeneration.

scholarly journals 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

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.

scholarly journals Protective Effects of Pinus halepensis Bark Extract and Nicotine on Cigarette Smoke-induced Oxidative Stress in Keratinocytes

In Vivo ◽  
2020 ◽  
Vol 34 (4) ◽  
pp. 1835-1843
Author(s):  
PANAGOULA PAVLOU ◽  
IOANNA ANTONIADOU ◽  
ASIMINA PERAKI ◽  
ANDREAS VITSOS ◽  
PARASKEVAS DALLAS ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Pinus Halepensis ◽  
Bark Extract ◽  
Protective Effects

scholarly journals Protective effects of a cocktail of lactic acid bacteria on microcystin-LR-induced hepatotoxicity and oxidative damage in BALB/c mice

RSC Advances ◽  
2017 ◽  
Vol 7 (33) ◽  
pp. 20480-20487 ◽  
Author(s):  
Jichun Zhao ◽  
Fengwei Tian ◽  
Qixiao Zhai ◽  
Ruipeng Yu ◽  
Hao Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Oxidative Damage ◽  
Protective Effects ◽  
And Oxidative Stress

The aim of this study was to investigate the effects of mixed lactic acid bacteria (LAB) against microcystin-LR-exposed hepatotoxicity and oxidative stress in BALB/c mice.

scholarly journals Melatonin reduces oxidative damage in mouse granulosa cells via restraining JNK-dependent autophagy

Reproduction ◽  
2018 ◽  
Vol 155 (3) ◽  
pp. 307-319 ◽  
Author(s):  
Yan Cao ◽  
Ming Shen ◽  
Yi Jiang ◽  
Shao-chen Sun ◽  
Honglin Liu
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Mammalian Cells ◽  
Therapeutic Strategies ◽  
Oxygen Species ◽  
Protective Effects ◽  
Follicular Atresia ◽  
Direct Role ◽  
Jnk Pathway

Oxidative stress-induced granulosa cell (GCs) injury is believed to be a common trigger for follicular atresia. Emerging evidence indicates that excessive autophagy occurs in mammalian cells with oxidative damage. N-acetyl-5-methoxytrypamine (melatonin) has been shown to prevent GCs from oxidative injury, although the exact mechanism remains to be elucidated. Here, we first demonstrated that the suppression of autophagy through the JNK/BCL-2/BECN1 signaling is engaged in melatonin-mediated GCs protection against oxidative damage. Melatonin inhibited the loss of GCs viability, formation of GFP-MAP1LC3B puncta, accumulation of MAP1LC3B-II blots, degradation of SQSTM1 and the expression of BECN1, which was correlated with impaired activation of JNK during oxidative stress. On the other hand, blocking of autophagy and/or JNK also reduced the level of H2O2-induced GCs death, but failed to further restore GCs viability in the presence of melatonin. Particularly, the suppression of autophagy provided no additional protective effects when GCs were pretreated with JNK inhibitor and/or melatonin. Importantly, we found that the enhanced interaction between BCL-2 and BECN1 might be a responsive mechanism for autophagy suppression via the melatonin/JNK pathway. Moreover, blocking the downstream antioxidant system of melatonin using specific inhibitors further confirmed a direct role of melatonin/JNK/autophagy axis in preserving GCs survival without scavenging reactive oxygen species (ROS). Taken together, our findings uncover a novel function of melatonin in preventing GCs from oxidative damage by targeting JNK-mediated autophagy, which might contribute to develop therapeutic strategies for patients with ovulation failure-related disorders.

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