Butein induction of HO-1 by p38 MAPK/Nrf2 pathway in adipocytes attenuates high-fat diet induced adipose hypertrophy in mice

2017 ◽  
Vol 799 ◽  
pp. 201-210 ◽  
Author(s):  
Zheng Wang ◽  
Sun-O Ka ◽  
Youngyi Lee ◽  
Byung-Hyun Park ◽  
Eun Ju Bae
Keyword(s):  
P38 Mapk ◽  
High Fat Diet ◽  
High Fat ◽  
Nrf2 Pathway

scholarly journals Keap1/Nrf2 pathway activation leads to a repressed hepatic gluconeogenic and lipogenic program in mice on a high-fat diet

2016 ◽  
Vol 591 ◽  
pp. 57-65 ◽  
Author(s):  
Stephen L. Slocum ◽  
John J. Skoko ◽  
Nobunao Wakabayashi ◽  
Susan Aja ◽  
Masayuki Yamamoto ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Nrf2 Pathway ◽  
Pathway Activation

scholarly journals Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Huadong Liu ◽  
Wei Xiong ◽  
Yu Luo ◽  
Hua Chen ◽  
Yaqiong He ◽  
...  
Keyword(s):  
P38 Mapk ◽  
High Fat Diet ◽  
Transforming Growth Factor ◽  
Elevated Serum ◽  
Serum Levels ◽  
Nuclear Antigen ◽  
High Fat ◽  
Aortic Plaque ◽  
Protein Levels ◽  
Progression Of Atherosclerosis

Background. Vascular remodeling is the most critical pathogenesis of atherosclerosis. Adipokine chemerin was known for its relationship with obesity as well as metabolism. Most recently, chemerin was found to play a crucial role in the pathologic process of cardiovascular diseases including coronary heart disease. In this study, we surveyed the role of chemerin in progression of atherosclerosis in ApoE−/− mice. Objective. To investigate the relationship between chemerin and progression of atherosclerosis in ApoE−/− mice and its mechanism. Methods. 8-week-old ApoE−/− mice were fed with high-fat diet to induce the atherosclerosis model. Adenoviruses were transfected for knockdown or overexpression of chemerin gene into aorta. Serums and aortic tissues of ApoE−/− mice were obtained after feeding high-fat diet for 16 weeks. HE staining and oil red staining were performed to evaluate aortic plaque. ELISA was performed to explore serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and transforming growth factor-β1 (TGF-β1). Real-time PCR and western blotting were carried out to investigate the mRNA and protein levels of chemerin, nuclear factor-κB p65 (NF-κBp65), proliferating cell nuclear antigen (PCNA), phosphorylated p38 mitogen-activated protein kinase (p-p38-MAPK), phosphorylated c-Jun N-terminal kinase (p-JNK), and phosphorylated extracellular signal regulated kinase 1/2 (p-ERK 1/2). Result. Aortic plaque formation was significantly induced by high-fat diet in ApoE−/− mice. Simultaneously, elevated serum levels of TNF-α and IL-1β and elevated mRNA and protein levels of chemerin, NF-κBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 were found in ApoE−/− mice. After aortic chemerin gene was inhibited by adenovirus, aortic atherosclerosis induced by high-fat diet was significantly meliorated, serum levels of TNF-α and IL-1β decreased, mRNA and protein levels of NF-κBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 decreased simultaneously. Conclusion. Our study revealed that chemerin stimulated the progression of atherosclerosis in ApoE−/− mice.

scholarly journals Restoration of 5-methoxytryptophan protects against atherosclerotic chondrogenesis and calcification in ApoE−/− mice fed high fat diet

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Guan-Lin Lee ◽  
Tsai-Lien Liao ◽  
Jing-Yiing Wu ◽  
Kenneth K. Wu ◽  
Cheng-Chin Kuo
Keyword(s):  
P38 Mapk ◽  
High Fat Diet ◽  
Chondrogenic Differentiation ◽  
Blue Staining ◽  
Calcium Deposition ◽  
Dependent Manner ◽  
High Fat ◽  
Phenotypic Switch ◽  
Mapk Activation ◽  
Atherosclerotic Lesions

Abstract Background Toll-like receptor-2 (TLR2) promotes vascular smooth muscle cell (VSMC) transdifferentiation to chondrocytes and calcification in a p38 MAPK-dependent manner. Vascular 5-methoxytryptophan (5-MTP) is a newly identified factor with anti-inflammatory actions. As 5-MTP targets p38 MAPK for its actions, we postulated that 5-MTP protects against vascular chondrogenesis and calcification. Methods High-fat diet-induced advanced atherosclerosis in mice were performed to investigate the effect of 5-MTP on atherosclerotic lesions and calcification. VSMCs were used to determine the role of 5-MTP in VSMC chondrogenic differentiation and calcification. Alizarin red S and Alcian blue staining were used to measure VSMC calcification and chondrogenic differentiation, respectively. Results 5-MTP was detected in aortic tissues of ApoE−/− mice fed control chow. It was reduced in ApoE−/− mice fed high-fat diet (HFD), but was restored in ApoE−/−Tlr2−/− mice, suggesting that HFD reduces vascular 5-MTP production via TLR2. Intraperitoneal injection of 5-MTP or its analog into ApoE−/− mice fed HFD reduced aortic atherosclerotic lesions and calcification which was accompanied by reduction of chondrogenesis and calcium deposition. Pam3CSK4 (Pam3), ligand of TLR2, induced SMC phenotypic switch to chondrocytes. Pretreatment with 5-MTP preserved SMC contractile proteins and blocked Pam3-induced chondrocyte differentiation and calcification. 5-MTP inhibited HFD-induced p38 MAPK activation in vivo and Pam3-induced p38 MAPK activation in SMCs. 5-MTP suppressed HFD-induced CREB activation in aortic tissues and Pam3-induced CREB and NF-κB activation in SMCs. Conclusions These findings suggest that 5-MTP is a vascular arsenal against atherosclerosis and calcification by inhibiting TLR2–mediated SMC phenotypic switch to chondrocytes and the consequent calcification. 5-MTP exerts these effects by blocking p38 MAPK activation and inhibiting CREB and NF-κB transactivation activity.

Calcium ameliorates obesity induced by high-fat diet and its potential correlation with p38 MAPK pathway

2011 ◽  
Vol 39 (2) ◽  
pp. 1755-1763 ◽  
Author(s):  
Chao Sun ◽  
Li Wang ◽  
Jun Yan ◽  
Shumin Liu
Keyword(s):  
P38 Mapk ◽  
High Fat Diet ◽  
Mapk Pathway ◽  
High Fat ◽  
P38 Mapk Pathway

Low-dose alcohol ameliorated high fat diet-induced anxiety-related behavior via enhancing adiponectin expression and activating the Nrf2 pathway

2021 ◽  
Author(s):  
Jie Cheng ◽  
Meng Zhang ◽  
Shaoli Cheng ◽  
Fan Li ◽  
Bingyi Zhang ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Low Dose ◽  
Obese Mice ◽  
High Fat ◽  
Nrf2 Pathway ◽  
Nrf2 Activation

Low-dose alcohol protected HFD-induced obese mice from the augmentation of anxiety-related behavior, which might be related to APN upregulation and Nrf2 activation.

Salvianolic Acid B Inhibits High-Fat Diet-Induced Inflammation by Activating the Nrf2 Pathway

2017 ◽  
Vol 82 (8) ◽  
pp. 1953-1960 ◽  
Author(s):  
Bin Wang ◽  
Jin Sun ◽  
Yonghui Shi ◽  
Guowei Le
Keyword(s):  
High Fat Diet ◽  
Salvianolic Acid B ◽  
High Fat ◽  
Nrf2 Pathway ◽  
Salvianolic Acid

scholarly journals Rosmarinic Acid, the Main Effective Constituent of Orthosiphon stamineus, Inhibits Intestinal Epithelial Apoptosis Via Regulation of the Nrf2 Pathway in Mice

Molecules ◽  
2019 ◽  
Vol 24 (17) ◽  
pp. 3027 ◽  
Author(s):  
Xuan Cai ◽  
Fan Yang ◽  
Lihui Zhu ◽  
Ye Xia ◽  
Qingyuan Wu ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
High Fat Diet ◽  
Rosmarinic Acid ◽  
Morphological Characteristics ◽  
Related Factor ◽  
Intestinal Epithelial ◽  
High Fat ◽  
Nrf2 Pathway ◽  
Orthosiphon Stamineus ◽  
Epithelial Cell Apoptosis

Many studies have shown that Orthosiphon stamineus extract (OE) has antioxidant activity, and we previously reported that OE protects the intestine against injury from a high-fat diet. However, the molecular mechanism underlying this protective effect of OE was unclear. Here, OE was separated according to polarity and molecular weight, and the antioxidant activity of each component was compared. The components with the highest antioxidant activity were analyzed by HPLC, which confirmed that rosmarinic acid (RA) was the main effective constituent in OE. OE and RA were then tested in a mouse high-fat diet-induced intestinal injury model. The antioxidant indices and morphological characteristics of the mouse jejunum were measured, and activation of the nuclear factor E2-related factor 2 (Nrf2) pathway and apoptosis of jejunal epithelial cells were analyzed. Of all the constituents in OE, RA contributed the most. Both RA and OE activated the Nrf2 pathway and increased downstream antioxidant enzyme activity. RA and OE protected the mouse intestine against high-fat diet-induced oxidative stress by preventing intestinal epithelial cell apoptosis via both extracellular and intracellular pathways. Thus, RA, the main effective constituent in OE, inhibits intestinal epithelial apoptosis by regulating the Nrf2 pathway in mice.

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