scholarly journals Krill Oil Inhibits NLRP3 Inflammasome Activation in the Prevention of the Pathological Injuries of Diabetic Cardiomyopathy

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 368
Author(s):  
Xuechun Sun ◽  
Xiaodan Sun ◽  
Huali Meng ◽  
Junduo Wu ◽  
Xin Guo ◽  
...  
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Nlrp3 Inflammasome ◽  
Cardiac Fibrosis ◽  
Inflammatory Cell ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Inflammasome Activation ◽  
Peroxisome Proliferator ◽  
Krill Oil ◽  
Peroxisome Proliferator Activated Receptor

Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus (DM), resulting in high mortality. Myocardial fibrosis, cardiomyocyte apoptosis and inflammatory cell infiltration are hallmarks of DCM, leading to cardiac dysfunction. To date, few effective approaches have been developed for the intervention of DCM. In the present study, we investigate the effect of krill oil (KO) on the prevention of DCM using a mouse model of DM induced by streptozotocin and a high-fat diet. The diabetic mice developed pathological features, including cardiac fibrosis, apoptosis and inflammatory cell infiltration, the effects of which were remarkably prevented by KO. Mechanistically, KO reversed the DM-induced cardiac expression of profibrotic and proinflammatory genes and attenuated DM-enhanced cardiac oxidative stress. Notably, KO exhibited a potent inhibitory effect on NLR family pyrin domain containing 3 (NLRP3) inflammasome that plays an important role in DCM. Further investigation showed that KO significantly upregulated the expression of Sirtuin 3 (SIRT3) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), which are negative regulators of NLRP3. The present study reports for the first time the preventive effect of KO on the pathological injuries of DCM, providing SIRT3, PGC-1α and NLRP3 as molecular targets of KO. This work suggests that KO supplementation may be a viable approach in clinical prevention of DCM.

scholarly journals Neuronal GPR30 Participates in Genistein-Mediated Neuroprotection in Ischemic Stroke by Inhibiting NLRP3 Inflammasome Activation in Ovariectomized Female Mice

2021 ◽  
Author(s):  
Shiquan Wang ◽  
Zhen Zhang ◽  
Jin Wang ◽  
Lina Ma ◽  
Jianshuai Zhao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Nlrp3 Inflammasome ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Receptor Protein ◽  
Inflammasome Activation ◽  
Peroxisome Proliferator ◽  
Neuroprotective Effects ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nlrp3 Inflammasome Activation

Abstract Estrogen replacement therapy (ERT) is potentially beneficial for the prevention and treatment of postmenopausal cerebral ischemia but inevitably increases the risk of cerebral hemorrhage and breast cancer when used for a long period of time. Genistein, a natural phytoestrogen, has been reported to contribute to the recovery of postmenopausal ischemic stroke with reduced risks. However, the underlying mechanism of genistein-mediated neuroprotection remains unclear. We reported that genistein exerted significant neuroprotective effects by enhancing the expression of neuronal G protein-coupled receptor 30 (GPR30) in the ischemic penumbra after cerebral reperfusion in ovariectomized (OVX) mice, and this effect was achieved through GPR30-mediated inhibition of nod-like receptor protein 3 (NLRP3) inflammasome activation. In addition, we found that Peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) was the pivotal molecule that participated in GPR30-mediated inhibition of NLRP3 inflammasome activation in OVX mice after ischemia/reperfusion (I/R) injury. Our data suggest that the neuronal GPR30/PGC-1α pathway plays an important role in genistein-mediated neuroprotection against I/R injury in OVX mice.

CBD Promotes Oral Ulcer Healing via Inhibiting CMPK2-Mediated Inflammasome

2021 ◽  
pp. 002203452110245
Author(s):  
X. Qi ◽  
W. Lin ◽  
Y. Wu ◽  
Q. Li ◽  
X. Zhou ◽  
...  
Keyword(s):  
Ulcer Healing ◽  
Nlrp3 Inflammasome ◽  
Therapeutic Potential ◽  
Inflammatory Lesion ◽  
Oral Ulcer ◽  
Inflammasome Activation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Oral Ulcers ◽  
Pyrin Domain

Oral ulcer is a common oral inflammatory lesion accompanied by severe pain but with few effective treatments. Cannabidiol (CBD) is recently emerging for its therapeutic potential in a range of diseases, including inflammatory conditions and cancers. Here we show that CBD oral spray on acid- or trauma-induced oral ulcers on mice tongue inhibits inflammation, relieves pain, and accelerates lesion closure. Notably, the enrichment of genes associated with the NOD, LRR, and NLRP3 pyrin domain–containing protein 3 (NLRP3) inflammasome pathway is downregulated after CBD treatment. The expression of cleaved-gasdermin D (GSDMD) and the percentage of pyroptotic cells are reduced as well. In addition, CBD decreases the expression of cytidine/uridine monophosphate kinase 2 (CMPK2), which subsequently inhibits the generation of oxidized mitochondria DNA and suppresses inflammasome activation. These immunomodulating effects of CBD are mostly blocked by peroxisome proliferator activated receptor γ (PPARγ) antagonist and partially antagonized by CB1 receptor antagonist. Our results demonstrate that CBD accelerates oral ulcer healing by inhibiting CMPK2-mediated NLRP3 inflammasome activation and pyroptosis, which are mediated mostly by PPARγ in the nucleus and partially by CB1 in the plasma membrane.

scholarly journals Long non-coding RNA Gm15441 attenuates hepatic inflammasome activation in response to PPARA agonism and fasting

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Chad N. Brocker ◽  
Donghwan Kim ◽  
Tisha Melia ◽  
Kritika Karri ◽  
Thomas J. Velenosi ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Metabolic Stress ◽  
Inflammasome Activation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Interacting Protein ◽  
Non Coding Rna ◽  
Nlrp3 Inflammasome Activation ◽  
Long Non Coding Rna

AbstractExploring the molecular mechanisms that prevent inflammation during caloric restriction may yield promising therapeutic targets. During fasting, activation of the nuclear receptor peroxisome proliferator-activated receptor α (PPARα) promotes the utilization of lipids as an energy source. Herein, we show that ligand activation of PPARα directly upregulates the long non-coding RNA gene Gm15441 through PPARα binding sites within its promoter. Gm15441 expression suppresses its antisense transcript, encoding thioredoxin interacting protein (TXNIP). This, in turn, decreases TXNIP-stimulated NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, caspase-1 (CASP1) cleavage, and proinflammatory interleukin 1β (IL1B) maturation. Gm15441-null mice were developed and shown to be more susceptible to NLRP3 inflammasome activation and to exhibit elevated CASP1 and IL1B cleavage in response to PPARα agonism and fasting. These findings provide evidence for a mechanism by which PPARα attenuates hepatic inflammasome activation in response to metabolic stress through induction of lncRNA Gm15441.

A Case of Bullous Amyloidosis Associated with an Inflammatory Cell Infiltration and Prominent Pruritus

2008 ◽  
Vol 70 (3) ◽  
pp. 269-273
Author(s):  
Taisuke KAMIYAMA ◽  
Yoshihiro KAWAGUCHI ◽  
Masami SASAKI ◽  
Masamichi SATOU ◽  
Kumiko MIURA ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration

scholarly journals The Symmetric 3D Organization of Connective Tissue around Implant Abutment: A Key-Issue to Prevent Bone Resorption

Symmetry ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1126
Author(s):  
Giovanna Iezzi ◽  
Francesca Di Lillo ◽  
Michele Furlani ◽  
Marco Degidi ◽  
Adriano Piattelli ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Connective Tissue ◽  
Inflammatory Cell ◽  
Soft Tissues ◽  
Three Dimensional ◽  
Collagen Fibers ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Oral Epithelium ◽  
Implant Abutment

Symmetric and well-organized connective tissues around the longitudinal implant axis were hypothesized to decrease early bone resorption by reducing inflammatory cell infiltration. Previous studies that referred to the connective tissue around implant and abutments were based on two-dimensional investigations; however, only advanced three-dimensional characterizations could evidence the organization of connective tissue microarchitecture in the attempt of finding new strategies to reduce inflammatory cell infiltration. We retrieved three implants with a cone morse implant–abutment connection from patients; they were investigated by high-resolution X-ray phase-contrast microtomography, cross-linking the obtained information with histologic results. We observed transverse and longitudinal orientated collagen bundles intertwining with each other. In the longitudinal planes, it was observed that the closer the fiber bundles were to the implant, the more symmetric and regular their course was. The transverse bundles of collagen fibers were observed as semicircular, intersecting in the lamina propria of the mucosa and ending in the oral epithelium. No collagen fibers were found radial to the implant surface. This intertwining three-dimensional pattern seems to favor the stabilization of the soft tissues around the implants, preventing inflammatory cell apical migration and, consequently, preventing bone resorption and implant failure. This fact, according to the authors’ best knowledge, has never been reported in the literature and might be due to the physical forces acting on fibroblasts and on the collagen produced by the fibroblasts themselves, in areas close to the implant and to the symmetric geometry of the implant itself.

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