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Carnosic Acid - Europe PMC

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Last Updated: 10 January 2023

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Carnosic acid inhibits secretion of allergic inflammatory mediators in IgE-activated mast cells via direct regulation of Syk activation.

Mast cells are the key mediators of inflammation that have long been recognized for their central role in allergic inflammatory disorders. Our company recently introduced rosemary extract as a potent regulator of mast cell functions, attenuating MAPK and NF-u03baB signaling, which was not widely distributed. Carnosic acid, a common polyphenolic component of RE-, has been shown to have anti-inflammatory activity in other immune cell models, but its role as a potential source of mast cell activation is unclear. Therefore, we wanted to determine the modulatory effects of CA in a mast cell model of allergic inflammation. In comparison to chemotherapy with CA, we sensitized bone marrow-derived mast cells with anti-trinitrophenyl IgE and stimulated with allergen under stem cell factor potentiation. Following IgE stimulation, we also see results from CA treatment, including the release of all cytokines and chemokines tested after IgE stimulation, and the detection of CCL2 gene expression, excepting CCL2.

Source link: https://europepmc.org/article/MED/36608933


Carnosic acid inhibits reactive oxygen species-dependent neutrophil extracellular trap formation and ameliorates acute respiratory distress syndrome.

Aims Infiltration of activated neutrophils into the lungs is a hallmark of acute respiratory distress syndrome. Carnosic acid is a food additive; however, its anti-neutrophilic activity in the treatment of ARDS has yet to be established; however, its anti-neutrophilic activity in the treatment of ARDS has yet to be demonstrated. The goal of this research is to show that CA can reduce ARDS by suppressing neutrophilic inflammation and oxidative damage. In a lipopolysaccharide-induced ARDS mouse model, the therapeutic effects of CA were determined. CA causes the reduction of extracellular regulated kinase and c-Jun N-terminal kinase in activated neutrophils, according to Mechanistic reports. This is consistent with the fact that CA is effective against ROS-dependent NET formation. In LPS-induced mice, CA treatment improved pulmonary neutrophil infiltration, oxidative damage, NET formation, and alveolar damage. Significance Our results point to the possibility of CA for neutrophil-associated ARDS therapy.

Source link: https://europepmc.org/article/MED/36587789


The chromosome-scale assembly of the Salvia rosmarinus genome provides insight into carnosic acid biosynthesis.

S. rosmarinus genome assembly at 1. 11 G in length is provided here; the genome contains 40,701 protein-coding genes; and the scaffold N50 value of 95. 5 Mb is given. S. rosmarinus, a 1. 5 MYA, demonstrated an independent whole genome duplication event in comparison to other diploid Labiatae. In S. rosmarinus, a transcriptomic acid content study of two S. rosmarinus cultivars with contrasting carnosic acid content showed 842 genes positively associated with carnosic acid biosynthesis. We propose a CA biosynthesis model in S. rosmarinus based on the genomes and these genes. The diterpene synthase and the cytochrome P450 family of CA synthesis-related genes form a biosynthetic gene cluster responsible for the production of leaf and root diterpenoids, which are found on S. rosmarinus chromosome 1 and 2, respectively.

Source link: https://europepmc.org/article/MED/36579923


Effects of rosmarinic acid, carnosic acid, rosmanol, carnosol, and ursolic acid on the pathogenesis of respiratory diseases.

This paper sought to identify preclinical and clinical studies investigating the effects of rosmarinic acid, carnosic acid, rosmanol, carnosol, and ursolic acid on allergic and immunologic disorders. RA may be a promising candidate for asthma therapy due to the suppression of the nuclear factor-u03baB pathway, the main factor in allergic asthma. In addition, CA has a significantly higher correlation with the nicotinic ACH receptor than a family of drugs that relax the smooth muscles, making it a potent antispasmodic therapy.

Source link: https://europepmc.org/article/MED/36564953


Controlled production of carnosic acid and carnosol in cell suspensions of Lepechinia meyenii treated with different elicitors and biosynthetic precursors.

Lepechinia meyenii is a medicinal plant that is used in the biosynthesis of various types of antioxidants, including the diterpenes carnosic acid and carnosol. Herein we present the results of plant tissue culture experiments in this medicinal plant, with particular emphasis on the design and evaluation of a cell suspension system for CA and CS production. Our findings revealed that the greatest accumulation of CA and CS was mainly due to oxidative stress, such as UV-light exposure polyethylene glycol NaCl, which mimic drought and saline stress, respectively. On days 18-24, CS optimized batch cultures containing 100 mg L -1 geranylgeraniol, 50 mg L -1 miltiradiene/abietatriene, and 5 g L -1 polyethylene glycol treated with 6 min UV light pulse resulted in an Acc max of 26. 7 mg L -1 for CA and 17. 3 mg L -1 for CS.

Source link: https://europepmc.org/article/MED/36562957


Carnosic acid suppressed the formation of NETs in alcoholic hepatosteatosis based on P2X7R-NLRP3 axis.

Alcoholic liver disease is characterized by a change in lipid metabolism and an inflammation reaction in the liver during the disease process. The alcoholic liver disease model was developed by Lieber-DeCarli control liquid feed plus a single binge with or without CA administration. CA's findings CA reduced lipid accumulation in mice's liver by reducing the expression of genes related to lipid synthesis, which was primarily responsible for lipid synthesis. CA reduced alcohol-induced immune cell infiltration in the liver and slowed the release of P2X7R-NLRP3 inflammasome, while blocking the formation of NETs in mouse liver tissue. CA attenuated the lipid accumulation triggered by ethanol stimulation, which was achieved by limiting the expression of SREBP1 and CA reduced the release of inflammatory factor IL-1u03b2 by inhibiting the transcription of P2X7R-NLRP3.

Source link: https://europepmc.org/article/MED/36577209

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions