scholarly journals Skrining Inhibitor NF-κB Combretum indicum dengan Metode Docking

2021 ◽  
Vol 18 (2) ◽  
pp. 157-163
Author(s):  
Samsul Hadi ◽  
Amalia Khairunnisa ◽  
Sefa Nur Khalifah ◽  
Sintya Oktaviani ◽  
Sri Oktaviana Sari ◽  
...  

Nuclear factor kappa B (NF-κB) is a transcription factor that regulates the expression of genes important for innate and adaptive immune responses. NF-κB overactivation is associated with inflammatory diseases such as autoimmune, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). This study aims to screen the chemical content of C.indicum against NF-κB-inducing kinase inhibitors. There are two methods used in this study, namely through PASSonline and docking. The docking method used was PLANTS. The results of PASSonline compounds that have P.a values above 0.7 weree arachidonic acid, linoleic acid, rutin, methyl urasolate, while the docking scores obtained were asquisqualic acid: -60.0382; arachidonic acid : -100,9410; linoleic acid: -93.8730; routine : -102,9320; methyl urasolate: -47,9166. This negative docking score indicates that the reaction between the compound and the target occurs easily. In conclusion, the compound predicted to have a potential as an inhibitor of NF-κB is Rutin.

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Anna Negroni ◽  
Salvatore Cucchiara ◽  
Laura Stronati

Intestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota. Moreover, IECs are strongly involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This review is focused on previous reports on different forms of cell death in intestinal epithelium.


2021 ◽  
Author(s):  
Doron Rimar ◽  
Merav Lidar ◽  
Nasrin Eiza ◽  
Adi D Sabag ◽  
Elias Toubi ◽  
...  

Abstract Background: Immune semaphorins are important players in controlling both innate and adaptive immune responses. The regulatory role of semaphorin3A (sema3A) in systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and other autoimmune diseases is widely reported. Decreased levels of serum sema3A were shown to be associated with SLE disease activity. Objectives: To assess urine concentrations of sema3A in SLE patients and its correlation with renal involvement and disease activity. Methods: Urine levels of sema3A were analyzed in 38 SLE patients of whom 13 had renal involvement and were compared to 10 healthy controls and 8 RA patients (disease control group). Results: The secretion of urine sema3A was found to be significantly lower in SLE patients compared to healthy controls and RA patients (4.9±3.9 ng/ml, 8.5±2.7 ng/ml, 9.85±1.7 ng/ml, respectively, p = 0.0006). Urine sema3A was significantly lower in SLE patients with lupus nephritis than in patients without nephritis (4.0±3.4 ng/ml vs 6.5±3.8 ng/ml, p=0.03). Urine sema3A was inversely correlated with proteinuria and SLE disease activity. Conclusion: Urine sema3A is decreased in lupus patients and should be further evaluated as a possible biomarker for disease activity and renal involvement.


2017 ◽  
Vol 214 (6) ◽  
pp. 1787-1808 ◽  
Author(s):  
Tizong Miao ◽  
Alistair L.J. Symonds ◽  
Randeep Singh ◽  
Janine D. Symonds ◽  
Ane Ogbe ◽  
...  

Egr2 and 3 are important for maintaining immune homeostasis. Here we define a fundamental function of Egr2 and 3 operating as a checkpoint that controls the transition between clonal expansion and differentiation of effector T cells. Egr2 and 3 deficiency resulted in defective clonal expansion but hyperactivation and excessive differentiation of T cells in response to viral infection. Conversely, sustained Egr2 expression enhanced expansion but severely impaired effector differentiation. Egr2 bound to and controlled the expression of genes regulating proliferation (Myc and Myb) and differentiation repressors (Bcl6, Id3), while repressing transcription factors required for effector function (Zeb2, RORa, RORc, and Bhlhe40). Egr2 and 3 expression in T cells was regulated reciprocally by antigen and IFNγ, providing a mechanism for adjusting proliferation and differentiation of individual T cells. Thus, Egr2 and 3 are upstream regulators of effector CD4 and CD8 T cells that are essential for optimal responses with limited immunopathology.


2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Young-Su Yi ◽  
Young-Jin Son ◽  
Chongsuk Ryou ◽  
Gi-Ho Sung ◽  
Jong-Hoon Kim ◽  
...  

Inflammation is a series of complex biological responses to protect the host from pathogen invasion. Chronic inflammation is considered a major cause of diseases, such as various types of inflammatory/autoimmune diseases and cancers. Spleen tyrosine kinase (Syk) was initially found to be highly expressed in hematopoietic cells and has been known to play crucial roles in adaptive immune responses. However, recent studies have reported that Syk is also involved in other biological functions, especially in innate immune responses. Although Syk has been extensively studied in adaptive immune responses, numerous studies have recently presented evidence that Syk has critical functions in macrophage-mediated inflammatory responses and is closely related to innate immune response. This review describes the characteristics of Syk-mediated signaling pathways, summarizes the recent findings supporting the crucial roles of Syk in macrophage-mediated inflammatory responses and diseases, and discusses Syk-targeted drug development for the therapy of inflammatory diseases.


2016 ◽  
Vol 9 ◽  
pp. CMAMD.S37477 ◽  
Author(s):  
Tsuyoshi Kasama ◽  
Airi Maeoka ◽  
Nao Oguro

Systemic lupus erythematosus (SLE) and related disorders are chronic inflammatory diseases characterized by abnormalities and, in some cases, even complete failure of immune responses as the underlying pathology. Although almost all connective tissue diseases and related disorders can be complicated by various neuropsychiatric syndromes, SLE is a typical connective tissue disease that can cause neurological and psychiatric syndromes. In this review, neuropsychiatric syndromes complicating connective tissue diseases, especially SLE are outlined, and pathological and other conditions that should be considered in the differential diagnosis are also discussed.


2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaofang Wang ◽  
Panpan Yi ◽  
Yuejin Liang

IL-36 is a member of the interleukin 1 cytokine family, which is currently experiencing a renaissance due to the growing understanding of its context-dependent roles and advances in our understanding of the inflammatory response. The immunological role of IL-36 has revealed its profound and indispensable functional roles in psoriasis, as well as in several inflammatory diseases, including inflammatory bowel disease (IBD), systemic lupus erythematosus, rheumatoid arthritis (RA) and cancer. More recently, an increasing body of evidence suggests that IL-36 plays a crucial role in viral, bacterial and fungal infections. There is a growing interest as to whether IL-36 contributes to host protective immune responses against infection as well as the potential implications of IL-36 for the development of new therapeutic strategies. In this review, we summarize the recent progress in understanding cellular expression, regulatory mechanisms and biological roles of IL-36 in infectious diseases, which suggest more specific strategies to maneuver IL-36 as a diagnostic or therapeutic target, especially in COVID-19.


2021 ◽  
Vol 11 ◽  
Author(s):  
Haruna Okude ◽  
Daisuke Ori ◽  
Taro Kawai

Recognition of pathogen-derived nucleic acids by pattern-recognition receptors (PRRs) is essential for eliciting antiviral immune responses by inducing the production of type I interferons (IFNs) and proinflammatory cytokines. Such responses are a prerequisite for mounting innate and pathogen-specific adaptive immune responses. However, host cells also use nucleic acids as carriers of genetic information, and the aberrant recognition of self-nucleic acids by PRRs is associated with the onset of autoimmune or autoinflammatory diseases. In this review, we describe the mechanisms of nucleic acid sensing by PRRs, including Toll-like receptors, RIG-I-like receptors, and DNA sensor molecules, and their signaling pathways as well as the disorders caused by uncontrolled or unnecessary activation of these PRRs.


2020 ◽  
Vol 21 (9) ◽  
pp. 3074
Author(s):  
Michele Dei Cas ◽  
Gabriella Roda ◽  
Feng Li ◽  
Francesco Secundo

Lipids are apolar small molecules known not only as components of cell membranes but also, in recent literature, as modulators of different biological functions. Herein, we focused on the bioactive lipids that can influence the immune responses and inflammatory processes regulating vascular hyperreactivity, pain, leukocyte trafficking, and clearance. In the case of excessive pro-inflammatory lipid activity, these lipids also contribute to the transition from acute to chronic inflammation. Based on their biochemical function, these lipids can be divided into different families, including eicosanoids, specialized pro-resolving mediators, lysoglycerophospholipids, sphingolipids, and endocannabinoids. These bioactive lipids are involved in all phases of the inflammatory process and the pathophysiology of different chronic autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, type-1 diabetes, and systemic lupus erythematosus.


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