Artemisinin attenuates intestinal epithelial barrier damage induced by LPS / 中国病理生理杂志
Chinese Journal of Pathophysiology
;
(12): 1285-1290, 2016.
Artículo
en Chino
| WPRIM
| ID: wpr-496549
ABSTRACT
[ ABSTRACT] AIM:
To investigate the effect of artemisinin on lipopolysaccharide ( LPS)-induced intestinal epi-thelial barrier damage in IEC-6 cells and its molecular mechanism.METHODS:
Cultured IEC-6 cells were divided to 5 groupscontrol group, LPS (100 mg/L) group and LPS +Artemisinin (30, 50 and 100μmol/L) groups.The cytotoxici-ty was detected by MTT assay.The releases of TNF-α, IL-1βand IL-6 in the IEC-6 cells were measured by ELISA.The transepithelial electrical resistance ( TER) was detected by electrical resistance tester, and the horseradish peroxidase (HRP) flux permeability were analyzed by a microplate reader.The expression of tight junction proteins, ZO-1, claudin-1 and occludin, and the expression of TLR4/MyD88/NF-κB at mRNA and protein levels were determined by RT-qPCR and Western blot.RESULTS:
Artemisinin alone (up to 100 μmol/L) or in combination with LPS (100 mg/L) was not toxic to IEC-6 cells.Compared with control group, the releases of TNF-α, IL-1βand IL-6 in the culture supernatant of IEC-6 cells significantly increased after treatment with LPS.The expression of TLR4/MyD88/NF-κB was activated by LPS.LPS down-regulated the protein expression of ZO-1, claudin-1 and occludin.However, artemisinin treatment decreased the re-leases of TNF-α, IL-1βand IL-6 in the culture supernatant of IEC-6 cells.The expression of TLR4/MyD88/NF-κB at mR-NA and protein levels was gradually reduced after treatment with artemisinin.In addition, artemisinin upregulated the pro-tein expression of ZO-1, claudin-1 and occludin significantly (P<0.01) in a dose-dependent manner.CONCLUSION:
Artemisinin attenuates LPS-induced intestinal epithelial barrier damage by inhibiting TLR4/MyD88/NF-κB activation in the IEC-6 cells.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Idioma:
Chino
Revista:
Chinese Journal of Pathophysiology
Año:
2016
Tipo del documento:
Artículo
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