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The phosphocholine head group in phospholipids of normal healthy cell membranes is not accessible but, when cells are damaged and die, enhanced availability of lysophosphatidylcholine and disruption of the lipid bilayer expose phosphocholine residues to which CRP avidly binds ( In acute respiratory distress syndrome (ARDS), there is extensive overproduction of free radicals and reduced extracellular and intracellular GSH leading to oxidative cell damage (108)

The anticancer mechanisms of SIN primarily involve the regulation of NF-B, tyrosine kinase, and STAT pathways, which inhibit the proliferation, invasion, and migration of tumor cells (93, 124, 125)

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