China
Africa
Explore chapters and articles related to this topic
The Role of Natural Products in COVID-19
Published in Hanadi Talal Ahmedah, Muhammad Riaz, Sagheer Ahmed, Marius Alexandru Moga, The Covid-19 Pandemic, 2023
Iqra Akhtar, Sumera Javad, Tehreema Iftikhar, Amina Tariq, Hammad Majeed, Asma Ahmad, Muhammad Arfan, M. Zia-Ul-Haq
In fact, these inflammasomes are responsible for deteriorated condition of COVID-19 patients and their multiple organ failure, leading to death. Inflammasomes are consisting of a number of immune protein with activated neutrophils and macrophages. Neutrophils are directly or indirectly involved in the formation of thrombus and an increase in the serum α thrombin level. This condition has been reported in COVID-19 patients [112, 113]. Cytokine reactive protein is produced and can cause cardiogenic shocks [114, 115].
Myocarditis
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
IL (interleukin)-1 is a pivotal proinflammatory cytokine amplifying the innate immune response. Upstream of IL-1 is the inflammasome, a cytosolic molecular structure composed of an adaptor protein, procaspase-1, and a sensor molecule. The best-characterized inflammasome has a sensor molecule called NLRP3 (nucleotide-binding domain and leucine-rich repeat pyrin domain containing-3). Biological treatments that block the IL-1 pathway, including the IL-Ra (IL-1 receptor antagonist) anakinra, the fully human IgG1 anti–IL-1β monoclonal antibody, canakinumab, and colchicine are potential candidates to treat myocarditis.
Nuclear Factor Kappa-B: Bridging Inflammation and Cancer
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Mohammad Aslam Khan, Girijesh Kumar Patel, Haseeb Zubair, Nikhil Tyagi, Shafquat Azim, Seema Singh, Aamir Ahmad, Ajay Pratap Singh
Inflammation is a protective immune response which helps to combat harmful entities like pathogens, irritants or dead cells. Inflammation is a highly regulated process and once it becomes deregulated, it may lead to many pathological conditions [78]. Innate immune response can be elicited by pathogen derived molecules, pathogen associated molecular patterns (PAMPs), or by danger-associated molecular patterns (DAMPs) generated through endogenous stress [78]. Inflammasome is a multiprotein complex, based on physiological and pathogenic stresses, responsible for the induction of inflammatory response. Inflammasome contains nucleotide-binding domain-like receptors (NLRs), absent in melanoma (AIM) and a zymogen, procaspase-1. Assembly of inflammasome leads to the activation of caspase-1, which enzymatically cleaves precursors of IL-1β and IL-18 to orchestrate the downstream inflammatory signals [78, 79]. Inflammasome-mediated immune response is highly regulated and it has been suggested that activation of NF-κB signaling pathway is required for the activation of NLRP3 inflammasome [80]. Recently, it has been shown that NF-κB signaling pathway can control excessive inflammatory response by restraining NLRP3 mediated inflammasome activation by inducing p62 dependent autophagy [81].
Bidirectional role of reactive oxygen species during inflammasome activation in acrolein-induced human EAhy926 cells pyroptosis
Published in Toxicology Mechanisms and Methods, 2021
Liping Jiang, Songsong Luo, Tianming Qiu, Qiannan Li, Chunteng Jiang, Xiance Sun, Guang Yang, Cong Zhang, Xiaofang Liu, Lijie Jiang
Emerging evidence supports that inflammasomes play a crucial role in the pathogenesis of cardiovascular diseases, especially atherosclerosis. After recognition of PAMPs, DAMPs, and environmental irritants, the inflammasomes increased the release of mature IL-1β and other members of the IL-1 family (Feng et al. 2020; Zhivaki and Kagan 2021). NLRP3 inflammasome has been studied more frequently than other NLR family members. Recently, NLRP3 inflammasome has been indicated to be involved in chlorpyrifos-induced HaCaT cytotoxicity(Jang et al. 2015). Elisabeth Wigenstam et al. reported that inhaled sulfur dioxide causes pulmonary and systemic inflammation in a rat model, accompanying by NLRP3 inflammasome activation (Wigenstam et al. 2016). These results suggest that several toxins can activate the NLRP3 inflammasome in many cell types. Consistently, our results demonstrated that acrolein trigger NLRP3 inflammasome activation and pyroptosis in EAhy926 cells, accompanying by caspase-1 cleavage and mature IL-1β production. Moreover, the knockdown of NLRP3 attenuated the acrolein-induced NLRP3 inflammasome activation and pyroptotic cell death (Figure 4).
Therapeutic plasma exchange with albumin: a new approach to treat Alzheimer’s disease
Published in Expert Review of Neurotherapeutics, 2021
Mercè Boada, Pablo Martínez-Lage, Pedro Serrano-Castro, Montserrat Costa, Antonio Páez
Microglial NLR family pyrin domain containing 3 (NLRP3) inflammasome activation has been extensively studied in acute and chronic central nervous system (CNS) disorders, including AD. Inflammasomes are intracellular multiprotein complexes that mediate innate immune responses. The NLRP3 inflammasome is formed by a sensor protein (NLRP3), an adaptor molecule (apoptosis-associated speck-like protein [ASC]), and an effector enzyme (caspase-1). Different stimuli activate the formation of the NLRP3 inflammasome complex, thereby initiating signaling cascades that promote the secretion of the proinflammatory mediators interleukin (IL)-1b and IL-18. This process is essential for the clearance of pathogens or injured cells. However, when dysregulated, it contributes to neuronal damage and neurodegeneration [27].
An overview of disease models for NLRP3 inflammasome over-activation
Published in Expert Opinion on Drug Discovery, 2021
Hongliang Zhang, Ayesha Zahid, Hazrat Ismail, Yujie Tang, Tengchuan Jin, Jinhui Tao
In recent years, many molecules were reported to modulate inflammasome signaling by interacting with different components of inflammasome complexes. However, the difficult reconstitution of the inflammasome in in vitro and in vivo settings has limited the development of specific on-target biochemical assays for compound activity confirmation and drug discovery in high throughput screening setups. The functions of NLRP3 inflammasome are diverse and regulating these processes by inhibiting NLRP3 is a very effective treatment. The current mainstream target drug sources mainly include computational synthesis based on target structure, chemical structure improvement based on existing drugs, and screening based on molecular libraries [40]. The efficiency of computational synthesis based on target structure is higher, but for a long time due to the lack of structures of NLRP3 and other component proteins, there were obstacles in structure-based design. In 2019, Nature reported the electron microscope structures of NLRP3 and NEK7 for the first time [41], which is expected to promote structure-based targeted drug design. Natural products are another important source of NLRP3 inhibitors and are widely used in Chinese medicine and can be used for clinical treatment once their effects are tested. There have been many articles summarizing the existing inhibitors of NLRP3 inflammasome [42–44].