Increased uterine NLRP3 inflammasome and leucocyte infiltration in a rat model of preeclampsia

2021 ◽  
Author(s):  
Huiqian Zeng ◽  
Xinjia Han ◽  
Zhiqin Zhu ◽  
Shengjun Yu ◽  
Shanshan Mei ◽  
...  
Keyword(s):  
Rat Model ◽  
Nlrp3 Inflammasome ◽  
Leucocyte Infiltration

scholarly journals Curcumin Reduces Neuronal Loss and Inhibits the NLRP3 Inflammasome Activation in an Epileptic Rat Model

2018 ◽  
Vol 15 (3) ◽  
pp. 186-192 ◽  
Author(s):  
Qianchao He ◽  
Lingfei Jiang ◽  
Shanshan Man ◽  
Lin Wu ◽  
Yueqiang Hu ◽  
...  
Keyword(s):  
Rat Model ◽  
Nlrp3 Inflammasome ◽  
Neuronal Loss ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

Expression of the NLRP3 Inflammasome in Cerebral Cortex After Traumatic Brain Injury in a Rat Model

2013 ◽  
Vol 38 (10) ◽  
pp. 2072-2083 ◽  
Author(s):  
Huan-Dong Liu ◽  
Wei Li ◽  
Zhen-Rui Chen ◽  
Yang-Chun Hu ◽  
Ding-Ding Zhang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Rat Model ◽  
Nlrp3 Inflammasome

scholarly journals Intra-articular Injection of Baicalein Inhibits Cartilage Catabolism and NLRP3 Inflammasome Signaling in a Posttraumatic OA Model

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Hui Bai ◽  
Rui Yuan ◽  
Zhiheng Zhang ◽  
Lin Liu ◽  
Xinyu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Nlrp3 Inflammasome ◽  
Type Ii Collagen ◽  
Cartilage Degeneration ◽  
Inflammasome Activation ◽  
Dependent Manner ◽  
Nlrp3 Inflammasome Activation ◽  
Immunochemical Staining

Baicalein has been shown to have chondroprotective potential in vitro. However, its effect on disease modification in osteoarthritis (OA) is largely unknown. The present study is aimed at determining whether baicalein could slow the progression of OA and inhibit OA-related inflammation in a rat model of destabilization of the medial meniscus (DMM) and the underlying mechanisms. The rats subjected to DMM surgery were treated with baicalein (0.8, 1.6, and 3.2 μg/L, 50 μL, once a week) by intra-articular injection for 6 weeks. Dexamethasone (0.4 mg/mL, 50 μL, once a week) was used as a positive control. Histologic grading of cartilage degeneration was performed using the Osteoarthritis Research Society International (OARSI) recommended grading system (on a scale of 0-6). The expression levels of molecules associated with cartilage homeostasis and inflammatory cytokines were analyzed; moreover, the NLRP3 inflammasome activation and cartilage oxidative stress-associated molecules were determined. Baicalein treatment reduced the OARSI score and slowed OA disease progression in a dose-dependent manner within a certain range. Compared with DMM rats, intra-articular injection of baicalein led to (1) reduced levels of inflammatory mediates such as IL-1β and TNF-α, (2) reduced immunochemical staining of MMP-13 and ADAMTS-5, (3) suppressed immunochemical staining loss of type II collagen, (4) reduced expression of cartilage degradation markers including CTX-II and COMP in urine, and (5) inhibited NLRP3 inflammasome activation rather than regulated expression of SOD, GSH, and MDA. In contrast to the administration of baicalein, dexamethasone injection showed similar effects to slow OA progression, while dexamethasone inhibited NLRP3 inflammasome partly through decreasing levels of SOD, GSH, and MDA. This study indicated that baicalein may have the potential for OA prevention and exerts anti-inflammatory effects partly via suppressing NLRP3 inflammasome activation without affecting oxidative stress-associated molecules, and inhibition of cartilage catabolism enzymes in an OA rat model.

scholarly journals URB597 protects against NLRP3 inflammasome activation by inhibiting autophagy dysfunction in a rat model of chronic cerebral hypoperfusion

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Shao-Hua Su ◽  
Yi-Fang Wu ◽  
Qi Lin ◽  
Da-Peng Wang ◽  
Jian Hai
Keyword(s):  
Proinflammatory Cytokines ◽  
Rat Model ◽  
Nlrp3 Inflammasome ◽  
Therapeutic Potential ◽  
Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Ultrastructural Changes ◽  
Inflammasome Activation ◽  
Related Proteins

Abstract Background Previous studies reported that URB597 (URB) had therapeutic potential for treating chronic cerebral hypoperfusion (CCH)-induced neuroinflammation and autophagy dysfunction. However, the interaction mechanisms underlying the CCH-induced abnormal excessive autophagy and neuroinflammation remain unknown. In this study, we investigated the roles of impaired autophagy in nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing (NLRP) 3 inflammasome activation in the rat hippocampus and the underlying mechanisms under the condition of induced CCH as well as the effect of URB treatment. Methods The CCH rat model was established by bilateral common carotid artery occlusion (BCCAo), and rats were randomly divided into 11 groups as follows: (1) sham-operated, (2) BCCAo; (3) BCCAo+autophagy inhibitor 3-methyladenine (3-MA), (4) BCCAo+lysosome inhibitor chloroquine (CQ), (5) BCCAo+microglial activation inhibitor minocycline, (6) BCCAo+ROS scavenger N-acetylcysteine (NAC), (7) BCCAo+URB, (8) BCCAo+URB+3-MA, (9) BCCAo+URB+CQ, (10) BCCAo+URB+minocycline, (11) BCCAo+URB+NAC. The cell localizations of LC3, p62, LAMP1, TOM20 and NLRP3 were assessed by immunofluorescence staining. The levels of autophagy-related proteins (LC3, p62, LAMP1, BNIP3 and parkin), NLRP3 inflammasome-related proteins (NLRP3, CASP1 and IL-1β), microglial marker (OX-42) and proinflammatory cytokines (iNOS and COX-2) were evaluated by western blotting, and proinflammatory cytokines (IL-1β and TNF-a) were determined by ELISA. Reactive oxygen species (ROS) were assessed by dihydroethidium staining. The mitochondrial ultrastructural changes were examined by electron microscopy. Results CCH induced microglial overactivation and ROS accumulation, promoting the activation of the NLRP3 inflammasome and the release of IL-1β. Blocked autophagy and mitophagy flux enhanced the activation of the NLRP3-CASP1 inflammasome pathway. However, URB alleviated impaired autophagy and mitophagy by decreasing mitochondrial ROS and microglial overactivation as well as restoring lysosomal function, which would further inhibit the activation of the NLRP3-CASP1 inflammasome pathway. Conclusion These findings extended previous studies indicating the function of URB in the mitigation of chronic ischemic injury of the brain.

scholarly journals Intermittent fasting therapy promotes insulin sensitivity by inhibiting NLRP3 inflammasome in rat model

2021 ◽  
Vol 10 (5) ◽  
pp. 5299-5309
Author(s):  
Bing-Jun Liang ◽  
Sheng-Rong Liao ◽  
Wei-Xuan Huang ◽  
Chao Huang ◽  
Hao Sheng Liu ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Rat Model ◽  
Nlrp3 Inflammasome ◽  
Intermittent Fasting

scholarly journals Resveratrol improves cardiac function and left ventricular fibrosis after myocardial infarction in rats by inhibiting NLRP3 inflammasome activity and the TGF-β1/SMAD2 signaling pathway

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11501
Author(s):  
Jinjin Jiang ◽  
Xiuping Gu ◽  
Huifeng Wang ◽  
Shibin Ding
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Signaling Pathway ◽  
Rat Model ◽  
Nlrp3 Inflammasome ◽  
Interstitial Fibrosis ◽  
Left Ventricular ◽  
Sham Operation ◽  
Protective Effects ◽  
Inflammasome Activity

Background Several studies have shown that resveratrol (RES), a naturally occurring polyphenol found in many plants, is beneficial for preventing cardiovascular diseases. However, the mechanism underlying the RES-mediated protection against myocardial infarction has not yet been revealed entirely. In this study, we investigated the protective effects of RES on cardiac function in a rat model of acute myocardial infarction (AMI) and the related underlying mechanisms. Methods Male Sprague-Dawley rats were randomly divided into four groups: Sham (sham operation), Sham-RES, AMI (AMI induction), and AMI-RES. The rat AMI model was established by the permanent ligation of left anterior descending coronary artery method. The rats in the RES-treated groups were gavaged with RES (50 mg/kg/day) daily for 45 days after the Sham operation or AMI induction; rats in the Sham and AMI groups were gavaged with deionized water. Cardiac function was evaluated by echocardiography. Atrial interstitial fibrosis was assessed by hematoxylin-eosin or Masson’s trichrome staining. Real-time PCR and western blotting analyses were performed to examine the levels of signaling pathway components. Results RES supplementation decreased the inflammatory cytokine levels, improved the cardiac function, and ameliorated atrial interstitial fibrosis in the rats with AMI. Furthermore, RES supplementation inhibited NLRP3 inflammasome activity, decreased the TGF-β1 production, and downregulated the p-SMAD2/SMAD2 expression in the heart. Conclusion RES shows notable cardioprotective effects in a rat model of AMI; the possible mechanisms underlying these effects may involve the improvement of cardiac function and atrial interstitial fibrosis via the RES-mediated suppression of NLRP3 inflammasome activity and inhibition of the TGF-β1/SMAD2 signaling pathway in the heart.

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