Abstract
The effects of antibiotics on the intestinal flora can create potential drug-drug interactions. The combination of amoxicillin and aspirin is high and there is a high probability of interaction. We used 16S rRNA, incubation experiments and liquid chromatography-tandem mass spectrometry to analyze rat biological samples to characterize the effect of amoxicillin on the pharmacokinetics of aspirin metabolites. We first discovered that amoxicillin reduced the species and number of intestinal flora in rats, such as reducing the abundance of Helicobacter pylori and Prevotella_copri. After 12, 24, and 36 hours of incubation, the remaining amount of aspirin in the aspirin and amoxicillin treatment groups decreased, and salicylic acid production increased, suggesting that aspirin is metabolized by the intestinal flora, and the main metabolite is salicylic acid. As the incubation time prolonged, the reduction of aspirin and the production of salicylic acid in the amoxicillin treatment group were slower. It is indicated that the metabolic activity of aspirin through the intestinal flora is slowed down after administration of amoxicillin. The pharmacokinetic experiments showed that after administration of amoxicillin, the area under the salicylic acid curve increased by 91.38%, the peak concentration increased by 60.43%, and the clearance rate decreased by 43.55%.The results demonstrated that amoxicillin affected the pharmacokinetics of aspirin active metabolite salicylic acid by slowing down the metabolic activity of intestinal flora on aspirin. The interaction between amoxicillin and aspirin mediated by the intestinal flora may affect the efficacy of aspirin and cause more significant adverse effects.
Highlights
The gut microflora is a large and diverse micro-ecological system, and the gut microbes maintain a dynamic balance between the organism and the body[1]
Based on the above background, we reasoned that the question: Does amoxicillin affect the biotransformation of aspirin by altering the metabolic activity of the intestinal flora? Does it affect the in vivo pharmacokinetics of aspirin? In order to solve the above problems, this experiment uses chromatographic techniques and microbiological analysis methods to study the interaction between amoxicillin and aspirin in pharmacokinetics, and provide experimental basis for clinical rational drug use
The results showed that the metabolism of aspirin in the intestinal flora of rats was slowed down after treatment with amoxicillin
Summary
The gut microflora is a large and diverse micro-ecological system, and the gut microbes maintain a dynamic balance between the organism and the body[1]. The external environment, pathological state of the body, and xenobiotics may cause dysbacteriosis, trigger various diseases, and even affect the metabolism and absorption of drugs, thereby affecting the clinical therapeutic effect[2,3,4]. Antibiotics can alter the intestinal flora, allowing bioconversion of other drugs used together before absorption in the gastrointestinal tract[5], which means that the effects of antibiotics on the intestinal flora produce potential drug-drug interactions (DDI). Aspirin is reported to be metabolized by the intestinal flora when passing through the gastrointestinal tract, and ampicillin affects the antithrombotic effect of aspirin by altering the intestinal flora[8]. In order to solve the above problems, this experiment uses chromatographic techniques and microbiological analysis methods to study the interaction between amoxicillin and aspirin in pharmacokinetics, and provide experimental basis for clinical rational drug use Based on the above background, we reasoned that the question: Does amoxicillin affect the biotransformation of aspirin by altering the metabolic activity of the intestinal flora? Does it affect the in vivo pharmacokinetics of aspirin? In order to solve the above problems, this experiment uses chromatographic techniques and microbiological analysis methods to study the interaction between amoxicillin and aspirin in pharmacokinetics, and provide experimental basis for clinical rational drug use
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