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High-Performance Liquid Chromatography
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Joel J. Kirschbaum, Adorjan Aszalos
Lavendamycin is a new antibiotic related to streptonigrin. To monitor the purification from fermentation broths, an octadecylsilane column was used with a mobile phase of 0.01 M potassium phosphate buffer, pH 8-acetonitrile (80:20) [453]. No other details were given.
Metal Ion Dependent Antibiotics in Chemotherapy
Published in Astrid Sigel, Helmut Sigel, Metal Ions in Biological Systems, 2004
David H. Petering, Chuanwu Xia, William E. Antholine
Streptonigrin is an aminoquinone antibiotic isolated from Streptomyces flocculus which displays significant antitumor properties as well as confounding host toxicity (Figure 8) [141]. The biological effects of the agent certainly include genotoxicity that may depend on the redox behavior of the drug or on its capacity to act as an inhibitor of topoisomerase II [142–144]. Its aminoquinone component is shared with other important drugs including actinomycin, mitomycin C and rifamycin. It is distinguished by the presence in its structure of several metal binding groups that confer on the drug the capacity to bind metal ions. Despite its interesting structure from a bioinorganic point of view, little systematic study of the compound has occurred [3].
Inhibiting the ROCK Pathway Ameliorates Acute Lung Injury in Mice following Myocardial Ischemia/reperfusion
Published in Immunological Investigations, 2022
Shang-Dian Liu, Yagudin Timur, Lei Xu, Wei-Xin Meng, Bo Sun, Dong-Yun Qiu
Paraffin sections were deparaffinized in xylene, dehydrated in ethanol, and rinsed in PBS for 5 min. Then, they were placed in 10% formaldehyde in PBS for 15 min and rinsed in PBS twice for 5 min each. Freshly prepared protease K working solution (100 μL) was dropped on the tissues, and the reaction was later terminated by washing the tissues in PBS for 5 min. Then, the tissue sections were incubated with 100 μL equilibration buffer at room temperature for 5 to 10 min after being washed in PBS and then incubated with 100 μL TdT at 37°C for 60 min in a wet box. The reaction was terminated by placing the tissue sections in 20× SSC solution at room temperature for 15 min, and then the sections were washed in 0.3% H2O2 in PBS for 3 to 5 min. Thereafter, anti-biotin streptonigrin horseradish peroxidase (HRP) solution diluted 1/500 was dropped onto the target region of each section, and after 30 min, the section was rinsed in PBS three times for 5 min each. Later, the sections were stained with diaminobenzidine (DAB), counterstained with hematoxylin and visualized by microscopy. The number of TUNEL-positive cells in each specimen was determined. For each experiment, staining was scored in five randomly selected areas of each specimen as follows: 0 = no cells stained; 1 = less than 10% of cells stained; 2 = 11–20% of cells stained; 3 = 21–40% of cells stained; and 4 = more than 40% of cells stained.
Screening of natural compounds identifies ferutinin as an antibacterial and anti-biofilm compound
Published in Biofouling, 2021
Shella Gilbert-Girard, Inés Reigada, Kirsi Savijoki, Jari Yli-Kauhaluoma, Adyary Fallarero
In total, 45 compounds were identified as active against planktonic cells and 26 of them were also active against biofilms. Of those 26 hits, 15 were compounds with a known antibiotic activity (actinomycin D, antibiotic A-23187, chelerythrine, chromomycin A3, coumermycin A1, lincomycin, mithramycin A, neomycin, nigericin, rifampicin, troleandomycin, narasin, streptonigrin, echinomycin and lasalocid A) and were therefore discarded. Five compounds (doxorubicin, ellipticine, etoposide, gliotoxin and gossypol) with well-reported cytotoxic effects, or low biocompatibility indices, were also discarded. Six hit compounds remained: honokiol, tschimganin, tschimganidin, ferutinin, oridonin and deoxyshikonin. Tschimganin (bornyl vanillate) has limited supply options and it did not seem to be cost-friendly (prices can be up to 100 € mg−1, although they can vary between regions), which made it a less interesting option for further developments as a potential antibacterial compound. Moreover, a more affordable and structurally related compound was identified (tschimganidin), and thus tschimganin was not studied further. The structures of the five selected hit compounds are presented in Figure 2.
Targeting citrullination in autoimmunity: insights learned from preclinical mouse models
Published in Expert Opinion on Therapeutic Targets, 2021
Ylke Bruggeman, Fernanda M.C. Sodré, Mijke Buitinga, Chantal Mathieu, Lut Overbergh, Maria J.L. Kracht
Pan-PAD inhibition, making use of Cl-amidine or BB-Cl-amidine, has been examined in several preclinical IBD models (Table 3). Dextran sulfate sodium (DSS)-induced colitis, a model for UC, displays increased citrullination in the colon resulting from an enhanced expression of both PAD2 and PAD4. PAD inhibition by Cl-amidine administration suppressed colitis and prevented epithelial DNA damage [78]. Cl-amidine appeared to suppress the oxidative burst in inflammatory cells and to specifically induce apoptosis. A follow-up study reported that BB-Cl-amidine showed an improved potency to suppress colitis compared to its first generation derivative Cl-amidine [81]. Although these results could not be reproduced in a recent study using Cl-amidine and the PAD4 inhibitor streptonigrin, this discrepancy may be attributed to the lower drug doses used and the shorter treatment regimen [82]. Also in a mouse model of CD, with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis, Cl-amidine effectively suppressed clinical symptoms [83]. This was associated with a reduced proinflammatory cytokine signature and decreased NET-associated proteins in the colon, supporting a role for neutrophils in disease onset and perpetuation. Given the protective effect of Cl-amidine on DNA damage in epithelium cells, its potential to prevent the development of CRC was explored. In addition to reduced colitis, tumorigenesis was significantly suppressed in azoxymethane (AOM)/DSS mice, a colitis-induced CRC model, after treatment with the pan-PAD inhibitor [84,85]. A substantial reduction in tumorigenesis, both in tumor size and number, was associated with reduced miRNA-16 levels in epithelial cells and decreased cell proliferation. Overall, these studies imply that inhibition of PADs in UC, CD and colitis-associated CRC can be a promising therapeutic target, for currently medically challenging diseases.