Search results for: Caspase 1ε
#33651308 
2021/03/02
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Anti-Inflammatory Activity of Melatonin: a Focus on the Role of NLRP3 Inflammasome.
Melatonin is a hormone of the pineal gland that contributes to the regulation of physiological activities, such as sleep, circadian rhythm, and neuroendocrine processes. Melatonin is found in several plants and has pharmacological activities including antioxidant, anti-inflammatory, hepatoprotective, cardioprotective, and neuroprotective. It also has shown therapeutic efficacy in treatment of cancer and diabetes. Melatonin affects several molecular pathways to exert its protective effects. The NLRP3 inflammasome is considered a novel target of melatonin. This inflammasome contributes to enhanced level of IL-1β, caspase-1 activation, and pyroptosis stimulation. The function of NLRP3 inflammasome has been explored in various diseases, including cancer, diabetes, and neurological disorders. By inhibiting NLRP3, melatonin diminishes inflammation and influences various molecular pathways, such as SIRT1, microRNA, long non-coding RNA, and Wnt/β-catenin. Here, we discuss these molecular pathways and suggest that melatonin-induced inhibition of NLRP3 should be advanced in disease therapy.Milad Ashrafizadeh, Masoud Najafi, Nasim Kavyiani, Reza Mohammadinejad, Tahereh Farkhondeh, Saeed Samarghandian
2372 related Products with: Anti-Inflammatory Activity of Melatonin: a Focus on the Role of NLRP3 Inflammasome.
100ug100.00 ul100.00 ul100.00 ug 50 UG0.1ml (1mg/ml)100.00 ul
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#33650689 2021/03/02
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Hyperglycemia accelerates inflammaging in the gingival epithelium through inflammasomes activation.
Diabetes accelerates inflammaging in various tissue with an increase in senescent cell burden and senescence-associated secretory phenotype (SASP) secretion, which is a significant cause of tissue dysfunction and contributes to the diabetic complications. Recently, inflammasomes are thought to contribute to inflammaging. Here, utilizing diabetic models in vivo and in vitro, we investigated the potential association between hyperglycemia-induced inflammaging and gingival tissue dysfunction and the mechanism underlying inflammasome-associated inflammaging.Peng Zhang, Boyao Lu, Rui Zhu, Dawei Yang, Weiqing Liu, Qian Wang, Ning Ji, Qianming Chen, Yi Ding, Xing Liang, Qi Wang
2978 related Products with: Hyperglycemia accelerates inflammaging in the gingival epithelium through inflammasomes activation.
2 mg100μg100ug125 Bags/Unit100ug
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#33649297 2021/03/01
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SARS-CoV-2 engages inflammasome and pyroptosis in human primary monocytes.
Infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with leukopenia and uncontrolled inflammatory response in critically ill patients. A better comprehension of SARS-CoV-2-induced monocyte death is essential for the identification of therapies capable to control the hyper-inflammation and reduce viral replication in patients with 2019 coronavirus disease (COVID-19). Here, we show that SARS-CoV-2 engages inflammasome and triggers pyroptosis in human monocytes, experimentally infected, and from patients under intensive care. Pyroptosis associated with caspase-1 activation, IL-1ß production, gasdermin D cleavage, and enhanced pro-inflammatory cytokine levels in human primary monocytes. At least in part, our results originally describe mechanisms by which monocytes, a central cellular component recruited from peripheral blood to respiratory tract, succumb to control severe COVID-19.André C Ferreira, Vinicius Cardoso Soares, Isaclaudia G de Azevedo-Quintanilha, Suelen da Silva Gomes Dias, Natalia Fintelman-Rodrigues, Carolina Q Sacramento, Mayara Mattos, Caroline S de Freitas, Jairo R Temerozo, Lívia Teixeira, Eugenio Damaceno Hottz, Ester A Barreto, Camila R R Pão, Lohanna Palhinha, Milene Miranda, Dumith Chequer Bou-Habib, Fernando A Bozza, Patrícia T Bozza, Thiago Moreno L Souza
2031 related Products with: SARS-CoV-2 engages inflammasome and pyroptosis in human primary monocytes.
25mg100ug Lyophilized20ug100ug Lyophilized100ug Lyophilized20ug100ug Lyophilized100 μg500 500 100 μg
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#33647825 2021/02/26
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Caspase-1 inhibition ameliorates murine acute graft versus host disease by modulating the Th1/Th17/Treg balance.
Our previous studies have implicated Caspase-1 signaling in driving the proinflammatory state of acute graft versus host disease (aGVHD). Therefore, we aimed to elucidate the mechanism of Caspase-1 in in murine models of aGVHD through specific inhibition of its activity with the decoy peptide Ac-YVAD-CMK. We transplanted bone marrow from donor C57BL/6 (H-2b) mice into recipient BALB/c (H-2Kd) mice and randomized the recipients into the following treatment cohorts: (1) allogeneic hematopoietic stem cell transplantation and splenic cell infusion control (PBS group); (2) low dose Ac-YVAD-CMK (AC low group); (3) and high dose Ac-YVAD-CMK (AC high group). Indeed, we observed that Caspase-1 inhibition by Ac-YVAD-CMK ameliorated pathological damage and inflammation in the liver, lungs, and colon elicited by aGVHD. This was associated with reduced mortality secondary to aGVHD. Mechanistically, we found that Caspase-1 inhibition modulated donor T cell expansion, restored the balance of Th1/Th17/Treg subsets, and markedly decreased serum levels and aGVHD target organ mRNA expression of IL-1β, IL-18, and HMGB1. Thus, we demonstrate that inhibition of Caspase-1 by Ac-YVAD-CMK mitigates murine aGVHD by regulating Th1/Th17/Treg balance and attenuating its characteristic proinflammatory state.Wei Chen, GuiZhen Su, Yan Xu, Wentong Guo, Rahul Bhansali, Bin Pan, QingLing Kong, Hai Cheng, Jiang Cao, KunMing Qi, Feng Zhu, Miao Li, ShengYun Zhu, LingYu Zeng, ZhenYu Li, Qingyun Wu, KaiLin Xu
2963 related Products with: Caspase-1 inhibition ameliorates murine acute graft versus host disease by modulating the Th1/Th17/Treg balance.
1000 assays100 ul100ug100ug1000 assays1000 assays50 ug50 ug 100ug200ul50 ug 1000 assays
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#33645621 2021/03/01
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Molecular mechanisms of An-Chuan Granule for the treatment of asthma based on a network pharmacology approach and experimental validation.
An-Chuan Granule (ACG), a traditional Chinese medicine (TCM) formula, is an effective treatment for asthma but its pharmacological mechanism remains poorly understood. In this study, network pharmacology was applied to explore the potential mechanism of ACG in the treatment of asthma. The tumor necrosis factor (TNF), toll-like receptor (TLR), and Th17 cell differentiation-related, nucleotide-binding oligomerization domain (NOD)-like receptor, and NF-kappaB pathways were identified as the most significant signaling pathways involved in the therapeutic effect of ACG on asthma. A mouse asthma model was established using ovalbumin (OVA) to verify the effect of ACG and the underlying mechanism. The results showed that ACG treatment not only attenuated the clinical symptoms, but also reduced inflammatory cell infiltration, mucus secretion and MUC5AC production in lung tissue of asthmatic mice. In addition, ACG treatment notably decreased the inflammatory cell numbers in bronchoalveolar lavage fluid (BALF) and the levels of pro-inflammatory cytokines (including IL-6, IL-17, IL-23, TNF-alpha, IL-1beta and TGF-beta) in lung tissue of asthmatic mice. In addition, ACG treatment remarkably down-regulated the expression of TLR4, p-P65, NLRP3, Caspase-1 and adenosquamous carcinoma (ASC) in lung tissue. Further, ACG treatment decreased the expression of receptor-related orphan receptor (RORγt) in lung tissue but increased that of Forkhead box (Foxp3). In conclusion, the above results demonstrate that ACG alleviates the severity of asthma in a "multi-compound and multi-target" manner, which provides a basis for better understanding of the application of ACG in the treatment of asthma.Xiao-Li Chen, Qing-Ling Xiao, Zhong-Hua Pang, Cheng Tang, Qi-Yong Zhu
2903 related Products with: Molecular mechanisms of An-Chuan Granule for the treatment of asthma based on a network pharmacology approach and experimental validation.
20 ug5mg
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#33645492 2021/03/01
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Dual Targeting of Autophagy and NF-κB Pathway by PPARγ Contributes to the Inhibitory Effect of Demethoxycurcumin on NLRP3 Inflammasome Priming.
Demethoxycurcumin (DMC), a natural derivative of curcumin, has anti-inflammatory activities. However, the mechanism has not been fully elucidated.Jing Tang, Xiaoxue Tan, Xiangmi Huang, Jie Zhang, Liang Chen, Aiyuan Li, Deming Wang
2775 related Products with: Dual Targeting of Autophagy and NF-κB Pathway by PPARγ Contributes to the Inhibitory Effect of Demethoxycurcumin on NLRP3 Inflammasome Priming.
5 G 25 MG100.00 ul1 module20 ul 25 ml Ready-to-use 1 module
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#33643422 2021/02/16
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Gegen Qinlian Decoction Ameliorates Nonalcoholic Fatty Liver Disease in Rats Oxidative Stress, Inflammation, and the NLRP3 Signal Axis.
Gegen Qinlian Decoction (GQD), a classic Chinese herbal formula, has been widely used in Chinese clinic for centuries and is well defined in treating nonalcoholic fatty liver disease (NAFLD). However, the mechanism action of GQD on NAFLD is still rarely evaluated. The present study aims to investigate the effect of GQD on treatment of NAFLD in rats and to further explore the underlying mechanism. The rat NAFLD model established by high-fat-diet feeding was used in the research. Our results exhibited the liver lesions and steatosis was significantly alleviated in NAFLD rats treated with GQD via Oil Red O and H&E staining. Body weight and liver index in GQD groups were reduced significantly ( < 0.05). Moreover, the biochemical analyzer test results showed that GQD significantly decreased blood lipid levels total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and liver injury indicators alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), while it increased the level of high-density lipoprotein cholesterol (HDL-C) ( < 0.05). The levels of interferon- (IFN-), tumor necrosis factor- (TNF-), and malondialdehyde (MDA) after the GQD treatment were significantly lower, and then interleukin-2 (IL-2), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were lifted significantly ( < 0.05). Further, GQD blocked the expression of NLRP3, ASC, caspase-1 mRNA, and proteins in the liver tissues significantly ( < 0.05). These findings indicated that GQD can ameliorate the hepatic steatosis and injury of NAFLD. Its possible mechanism involves the modulation of inflammatory cytokines and antioxidative stress and the inhibition of NLRP3 signal axis activation. The results support that GQD may be a promising candidate in the treatment of NAFLD.Yuqi Ying, Haitao Zhang, Dian Yu, Wei Zhang, Dongling Zhou, Shuangchun Liu
1205 related Products with: Gegen Qinlian Decoction Ameliorates Nonalcoholic Fatty Liver Disease in Rats Oxidative Stress, Inflammation, and the NLRP3 Signal Axis.
2 Pieces/Box4 Sample Kit2 Pieces/Box
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#33641439 //
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GLP-1 alleviates NLRP3 inflammasome-dependent inflammation in perivascular adipose tissue by inhibiting the NF-κB signalling pathway.
To study the effect of glucagon-like peptide 1 (GLP-1) on NLR family pyrin domain containing 3 (NLRP3) inflammasome-induced inflammation in perivascular adipose tissue (PVAT) of Zucker diabetic fatty (ZDF) rats and the underlying role of nuclear factor (NF)-κB signalling.Xiangheng Chen, Qiuling Huang, Juling Feng, Zhongsheng Xiao, Xiaoling Zhang, Lei Zhao
2306 related Products with: GLP-1 alleviates NLRP3 inflammasome-dependent inflammation in perivascular adipose tissue by inhibiting the NF-κB signalling pathway.
100 μg
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#33641435 2021/02/27
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Rosuvastatin corrects oxidative stress and inflammation induced by LPS to attenuate cardiac injury by inhibiting the NLRP3/TLR4 pathway.
The aim of the current study was to evaluate whether rosuvastatin was effective in attenuating cardiac injury in lipopolysaccharide(LPS)-challenged mice and H9C2 cells and identify the underlying mechanisms, focusing on the NLRP3/TLR4 pathway. Cardiac injury, cardiac function, apoptosis, oxidative stress, inflammatory response and the NLRP3/TLR4 pathway were evaluated in both in vivo and in vitro studies. LPS-induced cardiomyocytes injury was markedly attenuated by rosuvastatin treatment. Apoptosis was clearly ameliorated in myocardial tissue and H9C2 cells cotreated with rosuvastatin. In addition, excessive oxidative stress was present, as indicated by increases in MDA content, NADPH activity and ROS production and decreased SOD activity after LPS challenge. Rosuvastatin improved all the indicators of oxidative stress, with a similar effect to NAC(ROS scavenger). Notably, LPS-exposed H9C2 cells and mice showed significant NLRP3 and TLR4/NF-κB pathway activation. Administration of rosuvastatin reduced the increases in expression of NLRP3, ASC, pro-caspase-1, TLR4, and p65 and decreased the contents of TNF-α, IL-1β, IL-18 and IL-6, with a similar effect as MCC950 (NLRP3 inhibitor). In conclusion, inhibition of the inflammatory response and oxidative stress contributes to cardioprotection of rosuvastatin on cardiac injury induced by LPS, and the effect of rosuvastatin was achieved by inactivation of the NF-κB/NLRP3 pathway.Guocheng Ren, Qiujie Zhou, Meili Lu, Hongxin Wang