aminosalicylic acid
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2022 ◽  
pp. 96-97
Author(s):  
Anton C. de Groot
Keyword(s):  

2021 ◽  
Vol 29 ◽  
Author(s):  
Azzurra Chiara De Maio ◽  
Giovanna Basile ◽  
Domenico Iacopetta ◽  
Alessia Catalano ◽  
Jessica Ceramella ◽  
...  

Abstract: Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) mainly affecting the colon and the rectum. Its main characters are represented by relapsing and remitting mucosal inflammation, starting in the rectum and typically extending continuously proximally through part or the entire colon. UC pathogenesis depends on multiple factors, such as genetic predisposition, defects in the epithelial barrier, dysregulated immune responses, and environmental causes. The most frequent symptoms are abdominal pain, weight loss, mucus discharge, bloody diarrhoea, incontinence, nocturnal defecations, fever, and anemia. Existing therapies for UC include 5-aminosalicylic acid (5-ASA) and its derivatives, steroids, immunosuppressants and biological drugs. However, limited efficacy and unwanted adverse effects hardly limit these strategies of treatment. In the last decades, research studies have been driven towards complementary and alternative medicines for the treatment of UC. Various nutraceuticals have exhibited promising results in modulating intestinal inflammation meanwhile improving symptoms. These compounds possess a wide spectrum of positive health effects evidenced by in vitro studies, characterized by their involvement in antioxidant defenses, cell proliferation, and gene expression. The present review analyzes the available data about the different types of nutraceuticals and their potential effectiveness as adjuvant therapy of IBD, with particular emphasis to UC.


Pharmacology ◽  
2021 ◽  
pp. 1-7
Author(s):  
Atsuhito Kubota ◽  
Masaru Terasaki ◽  
Rie Takai ◽  
Masaki Kobayashi ◽  
Ryuta Muromoto ◽  
...  

<b><i>Introduction:</i></b> 5-Aminosalicylic acid (5-ASA) is widely used as a key drug in inflammatory bowel disease. It has been recently reported that 5-ASA induces CD4 + Foxp3 + regulatory T cells (Tregs) in the colon via the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that regulates inflammation. However, the role of 5-ASA as an AhR agonist that induces Tregs in the spleen remains unknown. <b><i>Methods:</i></b> In the present study, we investigated these themes using an AhR-mediated transactivation assay and flow cytometry analysis. The experiments were conducted by using DR-EcoScreen cells and C57BL/6 mice. <b><i>Results:</i></b> The DR-EcoScreen cell-based transactivation assay revealed that 5-ASA acted as a weak AhR agonist at concentrations of ≥300 μM (1.31–1.45-fold), and that a typical AhR agonist, 2,3,7,8-tetrachlorodibenzo-<i>p</i>-dioxin (TCDD), activated AhR at a concentration of 0.1 nM (22.8-fold). In addition, the treatment of mouse splenic cells with 300 μM 5-ASA in a primary culture assay significantly induced CD4+CD25 + Foxp3 + Tregs (control vs. 5-ASA: 9.0% vs. 12.65%, <i>p</i> &#x3c; 0.05), while 0.1 nM TCDD also showed significant induction of Tregs (control vs. TCDD: 9.0% vs. 14.1%, <i>p</i> &#x3c; 0.05). Interestingly, this induction was eliminated by co-treatment with an AhR antagonist, CH-223191. <b><i>Discussion:</i></b> These results suggest that 5-ASA is a weak agonist of AhR and thereby induces Tregs in spleen cells. Our findings may provide useful insights into the mechanism by which 5-ASA regulates inflammation.


2021 ◽  
Vol 25 (2) ◽  
Author(s):  
Hui Chen ◽  
Jinfeng Cui ◽  
Juan Wang ◽  
Yuan Wang ◽  
Fei Tong ◽  
...  

2021 ◽  
Vol 7 (12) ◽  
Author(s):  
Laura C. Gomes ◽  
Susana Campino ◽  
Cláudio R. F. Marinho ◽  
Taane G. Clark ◽  
Jody E. Phelan

Drug resistance in Mycobacterium tuberculosis , the causative agent of tuberculosis disease, arises from genetic mutations in genes coding for drug-targets or drug-converting enzymes. SNPs linked to drug resistance have been extensively studied and form the basis of molecular diagnostics and sequencing-based resistance profiling. However, alternative forms of functional variation such as large deletions and other loss of function (LOF) mutations have received much less attention, but if incorporated into diagnostics they are likely to improve their predictive performance. Our work aimed to characterize the contribution of LOF mutations found in 42 established drug resistance genes linked to 19 anti-tuberculous drugs across 32689 sequenced clinical isolates. The analysed LOF mutations included large deletions (n=586), frameshifts (n=4764) and premature stop codons (n=826). We found LOF mutations in genes strongly linked to pyrazinamide (pncA), isoniazid (katG), capreomycin (tlyA), streptomycin (e.g. gid) and ethionamide (ethA, mshA) (P<10−5), but also in some loci linked to drugs where relatively less phenotypic data is available [e.g. cycloserine, delaminid, bedaquiline, para-aminosalicylic acid (PAS), and clofazimine]. This study reports that large deletions (median size 1115 bp) account for a significant portion of resistance variants found for PAS (+7.1% of phenotypic resistance percentage explained), pyrazinamide (+3.5%) and streptomycin (+2.6%) drugs, and can be used to improve the prediction of cryptic resistance. Overall, our work highlights the importance of including LOF mutations (e.g. large deletions) in predicting genotypic drug resistance, thereby informing tuberculosis infection control and clinical decision-making.


2021 ◽  
Vol 12 ◽  
Author(s):  
Peishan Qiu ◽  
Lan Liu ◽  
Jun Fang ◽  
Meng Zhang ◽  
Haizhou Wang ◽  
...  

Background: Ulcerative colitis (UC) is a chronic recurrent disease of unknown etiology. Recently, it has been reported that autophagy-related gene polymorphism is closely associated with increased risk of UC, and the therapeutic effect of some UC drugs is mediated by regulating autophagy pathways. This study aims to identify pivotal autophagy-related regulators in UC pathogenesis and provide novel molecular targets for the treatment of active UC.Methods: Gene expression profiles and clinical information of active UC patients were obtained from GEO databases. CIBERSORT was adopted to evaluate the immune cell infiltration. We used weighted gene co-expression network analysis (WGCNA) and differential expression analysis to identify the pivotal modules and genes associated with active UC. Subsequently, we conducted validation in the validation set and explored its relationship with commonly used UC therapeutics.Results: 36 healthy controls and 46 active UC patients have been obtained from the training set of GSE53306, GSE87466, and GSE134025. There were 423 differentially expressed genes (DEGs) found, which dramatically enriched in autophagy-related pathways. And more infiltration of mast cells, activated T cells, dendritic cells, and M1 macrophages were observed in the intestinal mucosa of active UC, while more infiltration of resting immune cells and M2 macrophages in healthy controls. WGCNA indicated that the turquoise and blue modules were the critical modules. CASP1, SERPINA1, and CCL2 have been identified as the hub autophagy-related genes of active UC, after combining DEGs and 232 autophagy-related genes from HADb with the genes of turquoise and blue modules, respectively. We further verified that CASP1, SERPINA1, and CCL2 were positively associated with active UC and served as an autophagy-related biomarker for active UC. Moreover, increased SERPINA1 in the involved intestinal mucosa was reduced in patients with active UC who responded to golimumab or glucocorticoid therapy. But, neither CASP1, SERPINA1, and CCL2 were changed by treatment of 5-aminosalicylic acid (5-ASA) and azathioprine.Conclusion: CASP1, SERPINA1, and CCL2 are autophagy-related hub genes of active UC. And SERPINA1 may serve as a new pharmacological autophagy regulator of UC, which provides a new target for the use of small molecules targeting autophagy in the treatment of active UC.


2021 ◽  
Vol 18 ◽  
Author(s):  
Lin Yin ◽  
Yaru Xing ◽  
Xiaoqin Le ◽  
Jun Chen ◽  
Lin Zhang ◽  
...  

Background: To optimize therapy for patients with human immunodeficiency virus-tuberculosis (HIV-TB) coinfection, we developed an ultra-high-performance liquid chromatography/tandem mass spectrometry (UHPLC-MS) method to monitor seven second-line anti-tuberculosis drugs. Methods: Blood samples (n = 70) were collected from 35 patients with HIV-TB coinfection; the plasma sample was protein-precipitated and diluted with a solution containing heptafluorobutyric acid. The plasma concentrations of rifabutin (RBT), clofazimine (CLO), moxifloxacin (MFX), prothionamide (PTH), levofloxacin (LFX), amikacin (AMK), and para-aminosalicylic acid (PAS) were detected by UHPLC-MS/MS method. Results: In these 70 samples, the mean concentrations of RBT, CLO, MFX, PTH, LFX, and AMK were 173.8 (10.0–550.0), 61.1 (54.4–67.7), 646.6 (25.0–2480.0), 120.5 (50.0–597.0), 1565.9 (100.0–3480.0), and 10753.0 (400.0–76 700.0) µg/L, respectively. Only one sample was detected to have PAS with concentration less than the lower limit of quantification. Most of the drug concentrations detected in these patients were lower than the targeted concentrations in TB patients. Conclusion: We created a simple UHPLC-MS method for simultaneously quantifying anti-TB drugs. The plasma concentrations in HIV-TB co-infected patients were lower than the targeted concentrations. It is important to monitor anti-TB drugs in the future. This method will facilitate the monitoring of anti-TB drugs in the future.


Author(s):  
Suresh Suganya ◽  
Kandasamy Saravanan ◽  
Ramakrishnan Jaganathan ◽  
Poomani Kumaradhas

The intermolecular interactions and salt formation of acridine with 4-aminosalicylic acid, 5-chlorosalicylic acid and hippuric acid were investigated. The salts obtained were acridin-1-ium 4-aminosalicylate (4-amino-2-hydroxybenzoate), C13H10N+·C7H6NO3 − (I), acridin-1-ium 5-chlorosalicylate (5-chloro-2-hydroxybenzoate), C13H10N+·C7H4ClO3 − (II), and acridin-1-ium hippurate (2-benzamidoacetate) monohydrate, C13H10N+·C9H8NO3 −·H2O (III). Acridine is involved in strong intermolecular interactions with the hydroxy group of the three acids, enabling it to form supramolecular assemblies. Hirshfeld surfaces, fingerprint plots and enrichment ratios were generated and investigated, and the intermolecular interactions were analyzed, revealing their quantitative contributions in the crystal packing of salts I, II and III. A quantum theory of atoms in molecules (QTAIM) analysis shows the charge–density distribution of the intermolecular interactions. The isosurfaces of the noncovalent interactions were studied, which allows visualization of where the hydrogen-bonding and dispersion interactions contribute within the crystal.


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