Allopurinol
It works by reducing the production of uric acid, which can accumulate in the joints and cause painful inflammation.
Allopurinol is effective in lowering serum uric acid levels and reducing the frequency of gout flares.
It may also be used to prevent kidney stones associated with high uric acid levels.
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Most cited protocols related to «Allopurinol»
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Example 5
In examples of the invention, a bisBIA-producing yeast strain, that produces bisBlAs such as those generated using the pathway illustrated in (A), is engineered by integration of a single construct into locus YDR514C. Additionally,
The construct includes expression cassettes for P. somniferum enzymes 6OMT and CNMT expressed as their native plant nucleotide sequences. A third enzyme from P. somniferum, CPR, is codon optimized for expression in yeast. The PsCPR supports the activity of a fourth enzyme, Berberis stolonifera CYP80A1, also codon optimized for expression in yeast. The expression cassettes each include unique yeast constitutive promoters and terminators. Finally, the integration construct includes a LEU2 selection marker flanked by loxP sites for excision by Cre recombinase.
A yeast strain expressing Ps6OMT, PsCNMT, BsCYP80A1, and PsCPR is cultured in selective medium for 16 hours at 30° C. with shaking. Cells are harvested by centrifugation and resuspended in 400 μL breaking buffer (100 mM Tris-HCl, pH 7.0, 10% glycerol, 14 mM 2-mercaptoethanol, protease inhibitor cocktail). Cells are physically disrupted by the addition of glass beads and vortexing. The liquid is removed and the following substrates and cofactors are added to start the reaction: 1 mM (R,S)-norcoclaurine, 10 mM S-adenosyl methionine, 25 mM NADPH. The crude cell lysate is incubated at 30° C. for 4 hours and then quenched by the 1:1 addition of ethanol acidified with 0.1% acetic acid. The reaction is centrifuged and the supernatant analyzed by liquid chromatography mass spectrometry (LC-MS) to detect bisBlA products berbamunine, guattegaumerine, and 2′-norberbamunine by their retention and mass/charge.
We fitted linear regression models to the phenotypes, adjusting for sex, age, and the first 40 genetic principal components, as provided by the UK Biobank. For secondary analyses, the same models were additionally adjusted for 639 SNPs for eGFR28 (link), 63 SNPs for UACR9 (link), and 184 SNPs for urate18 (link) to account for the potential effect of common variants.
CKD and gout were defined using ICD10 codes from hospital inpatient records (N18.*, M10.*, UKB field 41270). Microalbuminuria was defined as UACR > 30 mg/g. ExWAS were carried out for these clinically relevant outcomes and used to annotate the findings for continuous kidney markers with respect to the direction and significance of their association with disease. To further characterize the risk allele carriers of selected trait-associated variants, kidney disease was additionally defined by ICD codes for acute kidney injury (N17.9), CKD (N18.3, N18.4, N18.5, N18.9), polycystic kidney disease (Q61.2, Q61.3), and another kidney (N28.1) or ureter (N39.0) disease. Information on allopurinol treatment was obtained from a verbal interview on medication usage.
The rats were randomly divided into five groups (each group of 8): blank control (BC) group; model control (MC) group; Allopurinol (ALL) group (10mg/kg/d); Wuling San high-dose group (WLS-HD, 630mg/kg/d); Wuling San low-dose group (WLS-LD, 315mg/kg/d). Potassium oxonate, Allopurinol, and Wuling San (capsule) were suspended in the 0.5% CMC-Na solution, respectively. The yeast extract was dissolved in pure water. In order to induce HUA, all groups except the BC group were intragastrically given PO (750 mg/kg /d) for 14 days. The model group was given 0.5% CMC-Na, the ALL group was given allopurinol treatment, and the WLS groups were given different WLS treatments via gavage, respectively. In contrast, the BC group received 0.5% CMC-Na in comparable volumes. In order to simulate the purine metabolism disorder caused by human consumption of high-purine food and increase UA levels, all groups except the BC group were intragastrically given yeast extract (10g/kg/d) on the same day; meanwhile, the BC group received pure water in comparable volumes.
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More about "Allopurinol"
This medication works by reducing the production of uric acid, which can accumulate in the joints and cause painful inflammation.
By lowering serum uric acid levels, allopurinol is effective at reducing the frequency of gout flares.
Xanthine, a purine metabolite, is the primary substrate for the enzyme xanthine oxidase.
This enzyme catalyzes the oxidation of xanthine to uric acid, the end product of purine metabolism.
Inhibiting xanthine oxidase, as allopurinol does, decreases the amount of uric acid produced and can help prevent the formation of painful uric acid crystals in the joints.
In addition to its use in treating gout, allopurinol may also be prescribed to prevent kidney stones associated with high uric acid levels.
The medication can help dissolve existing stones and reduce the risk of new stone formation.
Researchers can leverage the power of PubCompare.ai's AI-driven platform to easily locate and compare research protocols for allopurinol from a variety of sources, including scientific literature, preprints, and patents.
This optimization tool can help scientists make more informed decisions and streamline their studies, unlocking the future of protocol optimization today.
Other compounds that may be of interest in the context of allopurinol and uric acid metabolism include potassium oxonate, a uricase inhibitor; DMSO, a solvent with anti-inflammatory properties; quercetin, a natural flavonoid with antioxidant effects; DPPH, a free radical scavenging compound; and apocynin, an NADPH oxidase inhibitor.
Exploring the interactions and mechanisms of these related substances can provide valuable insights into the complex pathways involved in uric acid production and gout pathogenesis.