Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Geniposide, a Component of Gardenia Jasminoides Ellis, Inhibits NF-ĸb to Attenuate LPS-Induced Injury in Intestinal Epithelial Cells

Version 1 : Received: 6 January 2021 / Approved: 8 January 2021 / Online: 8 January 2021 (08:35:25 CET)

How to cite: Wang, Q.; Qiao, X.; Wang, M.; Jia, J.; Cui, A.Y. Geniposide, a Component of Gardenia Jasminoides Ellis, Inhibits NF-ĸb to Attenuate LPS-Induced Injury in Intestinal Epithelial Cells. Preprints 2021, 2021010130 (doi: 10.20944/preprints202101.0130.v1). Wang, Q.; Qiao, X.; Wang, M.; Jia, J.; Cui, A.Y. Geniposide, a Component of Gardenia Jasminoides Ellis, Inhibits NF-ĸb to Attenuate LPS-Induced Injury in Intestinal Epithelial Cells. Preprints 2021, 2021010130 (doi: 10.20944/preprints202101.0130.v1).

Abstract

The nuclear factor-ĸB (NF-ĸB) transcriptional system is a major effector pathway involved in inflammatory responses. Previous studies found that a Gardenia decoction (GD) inhibited the expression of NF-κB in a lipopolysaccharide (LPS)-stimulated mouse intestinal injury model. Herein, we hypothesized that geniposide (GE), a component of Gardenia jasminoides Ellis, also exerts anti-inflammatory effects and inhibits NF-ĸB activity in LPS-induced intestinal epithelial cells (IEC-6). IEC-6 cells were stimulated with LPS, following which the effects of GE on NF-ĸB signaling in the IEC-6 cells were examined by western blotting to detect IĸB phosphorylation/degradation. The expression of NF-κB was determined by immunofluorescence assay (IFA). Enzyme-linked immunosorbent assay (ELISA) was used to detect the inhibitory effect of GE on the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) activated by LPS in IEC-6 cells. In addition, the migration ability of IEC-6 cells was observed by the scratch method. These results showed that GE dose-dependently downregulated levels of the proinflammatory cytokines TNF-α, IL-6 and IL-1β that had been upregulated by LPS and suppressed the phosphorylation of IĸB and NF-ĸB induced by LPS. Our findings indicated that GE could reduce LPS-induced NF-ĸB signaling and proinflammatory expression in IEC-6 cells and significantly enhance the migration of IEC-6 cells. Moreover, GE inhibited the expression of NF-κB, nuclear transfer, and transcriptional activity in IEC-6 cells. GE could block the synthesis of inflammatory factors of IEC-6 cells by inhibiting activation of the IĸB/NF-κB signaling pathway induced by LPS.

Subject Areas

Geniposide; NF-ĸB; IEC-6; Signaling pathway; Cell migration

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