Protective Effects of Salidroside against Carbon Tetrachloride (CCl4)-Induced Liver Injury by Initiating Mitochondria to Resist Oxidative Stress in Mice

The antioxidant effect of salidroside has been proven, but its role in liver injury is poorly understood. In this study, we aimed to evaluate the protective effects and mechanism of salidroside on liver injury induced by carbon tetrachloride (CCl4) in vivo. Mice were pretreated with salidroside (60 mg/kg, intraperitoneally injected, i.p.) once per day for 14 consecutive days and then administered with CCl4 (15.95 g/kg, i.p.) for 24 h to produce a liver injury model. Salidroside attenuated hepatic transaminase elevation in serum and ameliorated liver steatosis and necrosis, thereby suggesting its protective effect on the liver. Salidroside antagonized CCl4-induced toxicity by equilibrating antioxidation system, thereby inhibiting reactive oxygen species accumulation, and restoring mitochondrial structure and function. Salidroside exerts antioxidant and liver-protective effects by selectively inhibiting the activation of genes, including growth arrest and DNA -damage-inducible 45 α (Gadd45a), mitogen-activated protein kinase 7 (Mapk7), and related RAS viral oncogene homolog 2 (Rras2), which induce oxidative stress in the mitogen-activated protein kinase pathway. These results revealed that salidroside can protect the liver from CCl4-induced injury by resisting oxidative stress and protecting mitochondrial function.

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Curcumin attenuates chronic ethanol-induced liver injury by inhibition of oxidative stress via mitogen-activated protein kinase/nuclear factor E2-related factor 2 pathway in mice

Pharmacognosy Magazine ◽

10.4103/0973-1296.165556 ◽

2015 ◽

Vol 11 (44) ◽

pp. 707 ◽

Cited By ~ 19

Author(s):

WeiGuo Dong ◽

ZhangE Xiong ◽

BaoYing Wang ◽

QiaoYun Tong ◽

ZhongYan Li

Keyword(s):

Oxidative Stress ◽

Protein Kinase ◽

Liver Injury ◽

Chronic Ethanol ◽

Mitogen Activated Protein Kinase ◽

Related Factor ◽

Nuclear Factor ◽

Mitogen Activated Protein

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Guanxintai Exerts Protective Effects on Ischemic Cardiomyocytes by Mitigating Oxidative Stress

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2017/4534387 ◽

2017 ◽

Vol 2017 ◽

pp. 1-10 ◽

Cited By ~ 2

Author(s):

Jing Yang ◽

Weiju Sun ◽

Junfeng Sun ◽

Fengyue Wang ◽

Yuling Hou ◽

...

Keyword(s):

Oxidative Stress ◽

Serum Lipid ◽

Antioxidative Activity ◽

Mitogen Activated Protein Kinase ◽

Protective Effects ◽

Myocardial Apoptosis ◽

Mitogen Activated Protein ◽

Underlying Mechanisms

Oxidative stress participates in numerous myocardial pathophysiological processes and is considered a therapeutic target for myocardial ischemia and heart failure. Guanxintai (GXT), a traditional Chinese medicine, is commonly used to treat cardiovascular disease on account of its numerous beneficial physiological activities, such as dilating coronary arteries, inhibiting platelet aggregation, and reducing the serum lipid content. However, the antioxidative properties of GXT and potential underlying mechanisms remain to be established. In the present study, we investigated the protective effects of GXT on ischemic cardiomyocytes and the associated antioxidative mechanisms, both in vivo and in vitro. Notably, GXT treatment reduced the degree of cardiomyocyte injury, myocardial apoptosis, and fibrosis and partially improved cardiac function after myocardial infarction. Furthermore, GXT suppressed the level of ROS as well as expression of NADPH oxidase (NOX) and phospho-p38 mitogen-activated protein kinase (MAPK) proteins. Our results collectively suggest that the protective effects of GXT on ischemic cardiomyocytes are exerted through its antioxidative activity of NOX inhibition.

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Resveratrol protects H9c2 embryonic rat heart derived cells from oxidative stress by inducing autophagy: role of p38 mitogen-activated protein kinase

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y2012-051 ◽

2012 ◽

Vol 90 (5) ◽

pp. 655-662 ◽

Cited By ~ 38

Author(s):

Xiao Cui Lv ◽

Hai Yan Zhou

Keyword(s):

Oxidative Stress ◽

Protein Kinase ◽

Cell Survival ◽

P38 Mapk ◽

Mapk Pathway ◽

Mitogen Activated Protein Kinase ◽

Protective Effects ◽

H9c2 Cells ◽

P38 Mapk Pathway ◽

Mitogen Activated Protein

Recently, many studies have attempted to illustrate the mechanism of autophagy in protection against oxidative stress to the heart induced by H2O2. However, whether resveratrol-induced autophagy involves the p38 mitogen-activated protein kinase (MAPK) pathway is still unknown. This study aimed to investigate whether treating H9c2 cells with resveratrol increases autophagy and attenuates the cell death and apoptosis induced by oxidative stress via the p38 MAPK pathway. Resveratrol with or without SB202190, an inhibitor of the p38 MAPK pathway, was added 30 min before H2O2. After H2O2 treatment, the cells were incubated under 5% CO2 at 37 °C for 24 h to assess cell survival and death or incubated for 20 min for Western blot and transmission electron microscopy. Flow cytometry was used to detect apoptosis after 6 h of H2O2 treatment. Resveratrol at 20 µmol/L protected H9c2 cells treated with 100 µmol/L H2O2 from oxidative damage. It increased cell survival and markedly decrease lactate dehydrogenase release. In addition, resveratrol increased autophagy and decreased H2O2-induced apoptosis. Furthermore, the protective effects of resveratrol were inhibited by 10 µmol/L SB202190. Thus, resveratrol protected H2O2-treated H9c2 cells by upregulating autophagy via the p38 MAPK pathway.

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Age-Related Changes in Activation of Mitogen-Activated Protein Kinase Cascades by Oxidative Stress

Journal of Investigative Dermatology ◽

10.1038/jidsp.1998.7 ◽

1998 ◽

Vol 3 (1) ◽

pp. 23-27 ◽

Cited By ~ 9

Author(s):

Kathryn Z Guyton ◽

Myriani Gorospe ◽

Xiantao Wang ◽

Yolanda D Mock ◽

Gertrude C Kokkonen ◽

...

Keyword(s):

Oxidative Stress ◽

Protein Kinase ◽

Mitogen Activated Protein Kinase ◽

Age Related ◽

Mitogen Activated Protein ◽

Age Related Changes

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Natural feed contaminant zearalenone decreases the expressions of important pro- and anti-inflammatory mediators and mitogen-activated protein kinase/NF-κB signalling molecules in pigs

British Journal Of Nutrition ◽

10.1017/s0007114513002675 ◽

2013 ◽

Vol 111 (3) ◽

pp. 452-464 ◽

Cited By ~ 38

Author(s):

Gina Cecilia Pistol ◽

Mihail Alexandru Gras ◽

Daniela Eliza Marin ◽

Florentina Israel-Roming ◽

Mariana Stancu ◽

...

Keyword(s):

Immune Response ◽

Protein Kinase ◽

Matrix Metalloproteinases ◽

Inflammatory Mediators ◽

Interferon Γ ◽

Mitogen Activated Protein Kinase ◽

Economic Point ◽

Mitogen Activated Protein ◽

Anti Inflammatory

Zearalenone (ZEA) is an oestrogenic mycotoxin produced byFusariumspecies, considered to be a risk factor from both public health and agricultural perspectives. In the presentin vivostudy, a feeding trial was conducted to evaluate thein vivoeffect of a ZEA-contaminated diet on immune response in young pigs. The effect of ZEA on pro-inflammatory (TNF-α, IL-8, IL-6, IL-1β and interferon-γ) and anti-inflammatory (IL-10 and IL-4) cytokines and other molecules involved in inflammatory processes (matrix metalloproteinases (MMP)/tissue inhibitors of matrix metalloproteinases (TIMP), nuclear receptors: PPARγ and NF-κB1, mitogen-activated protein kinases (MAPK): mitogen-activated protein kinase kinase kinase 7 (TAK1)/mitogen-activated protein kinase 14 (p38α)/mitogen-activated protein kinase 8 (JNK1)/ mitogen-activated protein kinase 9 (JNK2)) in the liver of piglets was investigated. The present results showed that a concentration of 316 parts per billion ZEA leads to a significant decrease in the levels of pro- and anti-inflammatory cytokines at both gene expression and protein levels, correlated with a decrease in the levels of other inflammatory mediators, MMP and TIMP. The results also showed that dietary ZEA induces a dramatic reduction in the expressions ofNF-κB1andTAK1/p38αMAPK genes in the liver of the experimentally intoxicated piglets, and has no effect on the expression ofPPARγmRNA. The present results suggest that the toxic action of ZEA begins in the upstream of the MAPK signalling pathway by the inhibition of TAK1, a MAPK/NF-κB activator. In conclusion, the present study shows that ZEA alters several important parameters of the hepatic cellular immune response. From an economic point of view, these data suggest that, in pigs, ZEA is not only a powerful oestrogenic mycotoxin but also a potential hepatotoxin when administered through the oral route. Therefore, the present results represent additional data from cellular and molecular levels that could be taken into account in the determination of the regulation limit of the tolerance to ZEA.

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