Daily low-dose aspirin taken before five nights of limited sleep reduces measurable markers of inflammation in the blood and immune cells when exposed to a bacterial stimulus.
Mechanism
Synthesis from 1 study
Aspirin blocks key enzymes in immune cells that trigger inflammation, which stops the production of signals that cause other inflammatory molecules to rise. This leads to lower levels of inflammation markers in the blood when sleep is restricted.
Most probable mechanism
Aspirin enters the bloodstream and permanently blocks enzymes in immune cells that make inflammatory chemicals. This stops the production of signals that tell the body to release more inflammation, leading to lower levels of inflammatory markers in the blood and reduced activity in immune cells when they encounter bacteria.
Acetylsalicylic acid is absorbed and deacetylated to salicylate, which irreversibly acetylates cyclooxygenase-1 and cyclooxygenase-2 enzymes in monocytes
Inhibition of cyclooxygenase enzymes reduces the conversion of arachidonic acid to prostaglandin H2, suppressing downstream pro-inflammatory eicosanoid production
Reduced prostaglandin signaling dampens NF-κB activation and suppresses transcription of interleukin-6 and other pro-inflammatory cytokines in monocytes
Lower interleukin-6 expression in monocytes reduces hepatic synthesis of C-reactive protein, decreasing systemic inflammation
Evidence from Studies
Supporting (1)
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0174 Using Low-Dose Acetylsalicylic Acid to Target Inflammation in Response to Experimental Sleep Restriction in Humans
Contradicting (0)
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