The milk-derived ACE-inhibitory peptide RLSFNP can cross the intestinal epithelium intact via the paracellular route, but its low permeability is primarily due to extensive hydrolysis.
Extensive hydrolysis limits RLSFNP bioavailability in vitro; leaves open its viability as an oral ACE inhibitor pending in vivo studies.
BACKGROUND To exert an antihypertensive effect after oral administration, angiotensin I‐converting enzyme (ACE)‐inhibitory peptides must remain active after intestinal transport. The purpose of this article is to elucidate the transport permeability and route of ACE‐inhibitory peptide Arg‐Leu‐Ser‐Phe‐Asn‐Pro (RLSFNP) across the intestinal epithelium using Caco‐2 cell monolayers. RESULTS Intact RLSFNP and RLSFNP breakdown fragments F, FNP, SFNP and RLSF were found in RLSFNP transport solution across Caco‐2 cell monolayers using ultra‐performance liquid chromatography–tandem mass spectrometry. RLSFNP fragments FNP, SFNP and RLSF also contributed to ACE inhibitory effects. Protease inhibitors (bacitracin and leupeptin) and absorption enhancers (sodium glycocholate hydrate, sodium deoxycholate and Na 2 EDTA) improved the transport flux of RLSFNP. A transport inhibitor experiment showed that intact RLSFNP may be transported via the paracellular route. CONCLUSION Intact RLSFNP can be transported across the Caco‐2 cell monolayers via the paracellular route. Extensive hydrolysis was the chief reason for the low permeability of RLSFNP.
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Guo et al. (2017) studied this question.
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