Abstract
The functional activity of dietary astaxanthin is closely related to its absorption, and the absorption of dietary carotenoids mainly mediated by transmembrane transport protein (TTP) has become the mainstream research direction in recent years. However, the main TTP mediating astaxanthin absorption and its potential mechanisms are still unclear. Hence, based on the preliminary screening results, this study aims to elucidate the role of cluster-determinant 36 (CD36) mediating astaxanthin absorption from the perspective of expression levels through in vitro cell model, in situ single-pass intestinal perfusion model and in vivo mice model. The results showed that astaxanthin uptake was significantly increased by 45.13% in CD36 overexpressing cells and decreased by 20.92% in the case of sulfo-N-succinimidyl oleate (SSO) inhibition. A similar trend also appeared in the duodenum and jejunum by in situ model. Moreover, astaxanthin uptake in the small intestine of CD36 knockout mice was significantly reduced by 88.22%. Furthermore, the inhibition or knockout of CD36 suppressed the expression of other transporters (SR-BI and NPC1L1). Interestingly, CD36 was also involved in the downstream secretion pathway, which is manifested by interfering with the expression of related proteins (ERK1/2, MTP, ApoB48, and ApoAI). Therefore, these results indicate the important role of CD36 in astaxanthin transmembrane transport for the first time, providing vital exploration way for the absorption of dietary fat-soluble substances.
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