scholarly journals Soluble Epoxide Hydrolase Pharmacological Inhibition Decreases Alveolar Bone Loss by Modulating Host Inflammatory Response, RANK-Related Signaling, Endoplasmic Reticulum Stress, and Apoptosis

2017 ◽  
Vol 361 (3) ◽  
pp. 408-416 ◽  
Author(s):  
Carlos Antonio Trindade-da-Silva ◽  
Ahmed Bettaieb ◽  
Marcelo Henrique Napimoga ◽  
Kin Sing Stephen Lee ◽  
Bora Inceoglu ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Bone Loss ◽  
Inflammatory Response ◽  
Endoplasmic Reticulum Stress ◽  
Epoxide Hydrolase ◽  
Alveolar Bone ◽  
Soluble Epoxide Hydrolase ◽  
Alveolar Bone Loss ◽  
Pharmacological Inhibition ◽  
Host Inflammatory Response

scholarly journals Inactivation of Cys 674 in SERCA2 increases BP by inducing endoplasmic reticulum stress and soluble epoxide hydrolase

2020 ◽  
Vol 177 (8) ◽  
pp. 1793-1805 ◽  
Author(s):  
Gang Liu ◽  
Fuhua Wu ◽  
Xiaoli Jiang ◽  
Yumei Que ◽  
Zhexue Qin ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase

scholarly journals Soluble Epoxide Hydrolase Deficiency or Inhibition Attenuates Diet-induced Endoplasmic Reticulum Stress in Liver and Adipose Tissue

2013 ◽  
Vol 288 (20) ◽  
pp. 14189-14199 ◽  
Author(s):  
Ahmed Bettaieb ◽  
Naoto Nagata ◽  
Daniel AbouBechara ◽  
Samah Chahed ◽  
Christophe Morisseau ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Adipose Tissue ◽  
Er Stress ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
Hepg2 Cells ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase ◽  
High Fat ◽  
Pharmacological Inhibition

Soluble epoxide hydrolase (sEH) is a cytosolic enzyme whose inhibition has beneficial effects in cardiovascular, inflammatory, and metabolic diseases in murine models. Mice with targeted deletion or pharmacological inhibition of sEH exhibit improved insulin signaling in liver and adipose tissue. Herein, we assessed the role of sEH in regulating endoplasmic reticulum (ER) stress in liver and adipose tissue. We report that sEH expression was increased in the livers and adipose tissue of mice fed a high fat diet, the adipose tissue of overweight humans, and palmitate-treated cells. Importantly, sEH deficiency or inhibition in mice attenuated chronic high fat diet-induced ER stress in liver and adipose tissue. Similarly, pharmacological inhibition of sEH in HepG2 cells and 3T3-L1 adipocytes mitigated chemical-induced ER stress and activation of JNK, p38, and cell death. In addition, insulin signaling was enhanced in HepG2 cells treated with sEH substrates and attenuated in cells treated with sEH products. In summary, these findings demonstrate that sEH is a physiological modulator of ER stress and a potential target for mitigating complications associated with obesity.

scholarly journals Inter-Relationship Between Rheumatoid Arthritis and Periodontitis

2014 ◽  
Vol 11 (1) ◽  
pp. 22-26 ◽  
Author(s):  
J Rajkarnikar ◽  
BS Thomas ◽  
SK Rao
Keyword(s):  
Rheumatoid Arthritis ◽  
Bone Loss ◽  
Inflammatory Response ◽  
Sedimentation Rate ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Gingival Index ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Erythrocyte Sedimentation

Background Periodontal medicine defines a rapidly emerging branch of Periodontology focusing on establishing a strong relationship between periodontal health and systemic health. It is speculated that the major common dysregulation which links Periodontitis with Rheumatoid arthritis (RA) is being played by the mediators of immune inflammatory response. Objectives To determine whether there is any relationship between periodontal disease and Rheumatoid arthritis. Methods A total of 100 patients were included for the present study which was divided into two groups: one group (cases) included 50 patients attending the Department of Orthopedics, Kasturba Medical College, Manipal who were diagnosed of Rheumatoid arthritis. Another subject population included 50 patients as controls attending the Department of Oral Medicine, Manipal College of Dental Sciences, Manipal with age and gender matched with those of rheumatoid arthritis group. Specific measures for periodontitis included plaque index, gingival index, number of missing teeth, and radiographic alveolar bone loss scores. Measures of rheumatoid arthritis included health assessment questionaires, levels of C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Various periodontal parameters were compared between the cases and controls. Results The average alveolar bone loss was statistically more severe in Rheumatoid arthritis (RA) group than in the controls although there were similar plaque index in both the groups. The gingival index was statistically higher in the RA group. The Erythrocyte Sedimentation Rate (ESR) and C- Reactive Protein (CRP) levels of RA patients were also significantly associated with the severity of periodontal disease. Conclusion There was a significant association between Rheumatoid arthritis and Periodontitis which may be due to a common underlying deregulation of the inflammatory response in these individuals. DOI: http://dx.doi.org/10.3126/kumj.v11i1.11018 Kathmandu University Medical Journal Vol.11(1) 2013: 22-26

EFFECTS OF ALENDRONATE THERAPY ON CYCLOSPORINE INDUCED ALVEOLAR BONE LOSS : A MORPHO-METRIC AND BIO-CHEMICAL STUDY IN RATS

2016 ◽  
Vol 4 (4) ◽  
pp. 947-955
Author(s):  
Sneha R Bhat ◽  
◽  
Aravind R Kudva ◽  
Dhoom S Mehta ◽  
◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Chemical Study ◽  
Alveolar Bone Loss

3,4,5-Trihydroxybenzoic acid attenuates ligature-induced periodontal disease in Wistar rats.

2020 ◽  
Vol 19 ◽  
Author(s):  
Ozkan Karatas ◽  
Fikret Gevrek
Keyword(s):  
Bone Loss ◽  
Gallic Acid ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Collagenase Activity ◽  
Osteoblastic Activity ◽  
Cell Counts ◽  
Experimental Periodontitis ◽  
Anti Inflammatory

Background: 3,4,5-Trihydroxybenzoic acid, which is also known as gallic acid, is an anti-inflammatory agent who could provide beneficial effects in preventing periodontal inflammation. The present study aimed to evaluate the anti-inflammatory effects of gallic acid on experimental periodontitis in Wistar rats. Alveolar bone loss, osteoclastic activity, osteoblastic activity, and collagenase activity were also determined. Methods: 32 Wistar rats were used in the present study. Study groups were created as following: Healthy control (C,n=8) group; periodontitis (P,n=8) group; periodontitis and 30 mg/kg gallic acid administered group (G30,n=8); periodontitis and 60 mg/kg gallic acid administered group (G60,n=8). Experimental periodontitis was created by placing 4-0 silk sutures around the mandibular right first molar tooth. Morphological changes in alveolar bone were determined by stereomicroscopic evaluation. Mandibles were undergone histological evaluation. Matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, bone morphogenetic protein (BMP)-2 expressions, tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and inflammatory cell counts were determined. Results: Highest alveolar bone loss was observed in the periodontitis group. Both doses of gallic acid decreased alveolar bone loss compared to the P group. TRAP-positive osteoclast cell counts were higher in the P group, and gallic acid successfully lowered these counts. Osteoblast cells also increased in gallic acid administered groups. Inflammation in the P group was also higher than those of C, G30, and G60 groups supporting the role of gallic acid in preventing inflammation. 30 and 60 mg/kg doses of gallic acid decreased MMP-8 levels and increased TIMP-1 levels. BMP levels increased in gallic acid administered groups, similar to several osteoblasts. Conclusion: Present results revealed an anti-inflammatory effect of gallic acid, which was indicated by decreased alveolar bone loss and collagenase activity and increased osteoblastic activity.

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