Aspersitin

Aspersitin

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Aspersitin
Category Antibiotics
Catalog number BBF-00113
CAS 86996-89-6
Molecular Weight 267.32
Molecular Formula C14H21NO4

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Description

Aspersitin is an antibiotic produced by Aspergillus parasiticus. It has anti-gram-positive and negative bacteria activity.

Specification

IUPAC Name (6R)-5-amino-6-hydroxy-3-methoxy-2,6-dimethyl-4-[(2S)-2-methylbutanoyl]cyclohexa-2,4-dien-1-one
Canonical SMILES CCC(C)C(=O)C1=C(C(C(=O)C(=C1OC)C)(C)O)N
InChI InChI=1S/C14H21NO4/c1-6-7(2)10(16)9-11(19-5)8(3)13(17)14(4,18)12(9)15/h7,18H,6,15H2,1-5H3/t7-,14+/m0/s1
InChI Key UYJPMNCMOPWWNM-JKYUHCHBSA-N

Properties

Antibiotic Activity Spectrum Gram-positive bacteria; Gram-negative bacteria; mycobacteria
Melting Point 58-60°C

Reference Reading

1. Platelet depletion does not alter the course of Brucella abortus infection in vivo
Berny Arias-Gómez, Roger Fonseca-Muñoz, Alejandro Alfaro-Alarcón, Carlos Chacón-Díaz, Edgardo Moreno, Alexandra Rucavado, Elías Barquero-Calvo Microb Pathog. 2022 Mar;164:105458. doi: 10.1016/j.micpath.2022.105458. Epub 2022 Feb 25.
Brucellosis is a bacterial disease of animals and a zoonotic infection. Thrombocytopenia is a common outcome in long-lasting brucellosis in humans. Likewise, ex vivo experiments have shown that platelets may play a role in Brucella abortus infections. Following these reports, we explored the course of brucellosis in thrombocytopenic mice, using the non-toxic low-molecular-weight aspercetin protein that depletes platelets in vivo. Aspercetin does not induce systemic hemorrhage or inflammation, and when injected into mice, it generates a rapid dose-dependent drop in platelet counts without affecting central organs, disrupting hematological parameters, or the proinflammatory cytokine profile. Compared to the B. abortus infected control group, the infected thrombocytopenic mice did not show significant differences in the hematological profiles, pathological score, spleen, liver histopathology, or bacterial loads. Except for IL-6, which was higher in the infected thrombocytopenic mice, the TNF-α, IFN-γ and IL-10 did not significantly differ with the PBS-infected group. The results indicate that platelets do not play a significant role in modulating Brucella infection in vivo at the early stages of infection, which is commensurate with the stealthy strategy followed by Brucella organisms at the onset of the disease.
2. Platelet depletion enhances lethal, hemorrhagic and myotoxic activities of Bothrops asper snake venom in a murine model
Andrea Ulloa-Fernández, Teresa Escalante, José María Gutiérrez, Alexandra Rucavado Toxicon. 2022 Nov;219:106936. doi: 10.1016/j.toxicon.2022.106936. Epub 2022 Oct 3.
Platelets play key roles in hemostasis, inflammation, immune response, and tissue repair. Although it is known that viperid snake venoms induce thrombocytopenia and platelet hypoaggregation, the roles of these effects in the overall outcome of envenoming are poorly known. This study aimed to assess the effect of platelet depletion on several toxic activities induced by the venom of the Central American viperid snake Bothrops asper in a mouse model. A profound thrombocytopenia was induced in mice by the administration of aspercetin, a C-type lectin-like protein that induces platelet agglutination and drop in platelet counts, while a control group was treated with saline solution instead. Upon envenoming, animals rendered thrombocytopenic developed a higher extent of local and systemic hemorrhage and local myonecrosis, as compared to control envenomed mice. In addition, the median lethal dose (LD50), determined by the intraperitoneal route, was significantly lower in thrombocytopenic mice, underscoring a higher toxicity of venom in these conditions. No difference in the value of LD50 between the two groups was observed when using the intravenous route of injection, and no difference was observed in the magnitude and time-course of footpad edema. Skeletal muscle regeneration was assessed 14 days after venom injection in muscle. Both experimental groups showed a similarly poor regeneration, suggesting that platelets do not play a key role in the regenerative process in these experimental conditions. Results indicate that depletion of platelets increases hemorrhagic and myotoxic effects, as well as overall toxicity, of B. asper venom, implying that platelets play a protective hemostatic role in this model of envenoming.
3. Thrombocytopenia and platelet hypoaggregation induced by Bothrops asper snake venom. Toxins involved and their contribution to metalloproteinase-induced pulmonary hemorrhage
Alexandra Rucavado, Mónica Soto, Teresa Escalante, Gilbert D Loría, Raghuvir Arni, José María Gutiérrez Thromb Haemost. 2005 Jul;94(1):123-31. doi: 10.1160/TH05-02-0112.
Thrombocytopenia and platelet dysfunction occur in patients bitten by Bothrops sp snakes in Latin America. An experimental model was developed in mice to study the effects of B. asper venom in platelet numbers and function. Intravenous administration of this venom induces rapid and prominent thrombocytopenia and ex vivo platelet hypoaggregation. The drop in platelet numbers was primarily due to aspercetin, a protein of the C-type lectin family which induces von Willebrand factor-mediated platelet aggregation/agglutination. In addition, the effect of class P-III hemorrhagic metalloproteinases on the microvessel wall also contributes to thrombocytopenia since jararhagin, a P-III metalloproteinase, reduced platelet counts. Hypoaggregation was associated with the action of procoagulant and defibrin(ogen)ating proteinases jararacussin-I (a thrombin-like serine proteinase) and basparin A (a prothrombin activating metalloproteinase). At the doses which induced hypoaggregation, these enzymes caused defibrin(ogen)ation, increments in fibrin(ogen) degradation products and D-dimer and prolongation of the bleeding time. Incubation of B. asper venom with batimastat and alpha2-macroglobulin abrogated the hypoaggregating activity, confirming the role of venom proteinases in this effect. Neither aspercetin nor the defibrin(ogen)ating and hypoaggregating components induced hemorrhage upon intravenous injection. However, aspercetin, but not the thrombin-like or the prothrombin-activating proteinases, potentiated the hemorrhagic activity of two hemorrhagic metalloproteinases in the lungs.

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