Solanum melongena L. Extract Promotes Intestinal Tight Junction Re-Assembly via SIRT-1-Dependent Mechanisms
Issued Date
2024-01-01
Resource Type
ISSN
16134125
eISSN
16134133
Scopus ID
2-s2.0-85200050380
Journal Title
Molecular Nutrition and Food Research
Rights Holder(s)
SCOPUS
Bibliographic Citation
Molecular Nutrition and Food Research (2024)
Suggested Citation
Sukmak P., Kulworasreth P., Treveeravoot S., Arinno A., Anuwongworavet S., Wachiradejkul W., Kulworasreth P., Teansuk N., Thongnak L., Amonlerdpison D., Inchai J., Jakrachai C., Akrimajirachoote N., Aonbangkhen C., Muanprasat C., Poolsri W., Vaddhanaphuti C.S., Pongkorpsakol P. Solanum melongena L. Extract Promotes Intestinal Tight Junction Re-Assembly via SIRT-1-Dependent Mechanisms. Molecular Nutrition and Food Research (2024). doi:10.1002/mnfr.202400230 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/100408
Title
Solanum melongena L. Extract Promotes Intestinal Tight Junction Re-Assembly via SIRT-1-Dependent Mechanisms
Corresponding Author(s)
Other Contributor(s)
Abstract
Tight junction disruption can lead to pathogenesis of various diseases without therapeutic strategy to recover intestinal barrier integrity. The main objective of this study is to demonstrate the effect of Solanum melongena L. extract (SMLE) on intestinal tight junction recovery and its underlying mechanism. Intestinal barrier function is attenuated by Ca2+ depletion. SMLE treatment increased TER value across T84 cell monolayers. Permeability assay reveals that Ca2+ depletion promotes 4-kDa FITC-dextran permeability, but not 70-kDa FITC-dextran. SMLE suppresses the rate of 4-kDa FITC-dextran permeability, indicating that SMLE inhibits paracellular leak pathway permeability. SMLE-mediated TER increase and leak pathway suppression are abolished by neither calcium/calmodulin-dependent protein kinase kinase β (CaMKKβ) inhibitor nor AMP-activated protein kinase (AMPK) inhibitor. Furthermore, mammalian target of rapamycin (mTOR) and extracellular signal-regulated kinase (ERK) inhibitors have no effects on SMLE-mediated TER increase and leak pathway suppression. Interestingly, SMLE is unable to enhance TER value and diminish leak pathway permeability in T84 cell monolayers pre-treated with sirtuin-1 (SIRT-1) inhibitor. Immunofluorescence staining reveals that SMLE enhances re-assembly of tight junction proteins, including occludin and ZO-1 to intercellular space but this effect is abolished by SIRT-1 inhibitor. These data suggest that SMLE promotes intestinal tight junction re-assembly via SIRT-1-dependent manner.