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Background: Ginsenoside Rg1 has been studied to improve systemic inflammatory injury induced by sepsis, but its mechanism is not fully understood. The objective of this study was to explore the potential molecular mechanism by which Rg1 ameliorates septic intestinal barrier function impairment.
Results: Rg1 administration or miR-30e-5p upregulation alleviated LPS-induced apoptosis of Caco2 cells, decreased LDH and inflammatory cytokines levels, enhanced cell proliferation, promoted tight junction protein expression, and inhibited p65 phosphorylation. These beneficial effects of Rg1 were compensated by miR-30e-5p knockdown or FBXO11 overexpression. Animal studies have also yielded consistent results. Mechanistically, Rg1 performed this role by upregulating miR-30e-5p and inhibiting FBXO11 expression.
Conclusions: Rg1 protects intestinal barrier function in sepsis by regulating the miR-30e-5p/FBXO11 axis. These data provide new insights into the development of targeted agents for septic intestinal injury and the understanding of Rg1's therapeutic mechanisms.
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