Αρχειοθήκη ιστολογίου

Τετάρτη 22 Δεκεμβρίου 2021

Protective effects of syringic acid on inflammation, apoptosis and intestinal barrier function in Caco-2 cells following oxygen-glucose deprivation/reoxygenation-induced injury

xlomafota13 shared this article with you from Inoreader

Exp Ther Med. 2022 Jan;23(1):66. doi: 10.3892/etm.2021.10989. Epub 2021 Nov 23.

ABSTRACT

Syringic acid (SA) is an abundant phenolic acid compound that has been demonstrated to yield therapeutic benefits in myocardial and renal ischemia/reperfusion (I/R). However, the role of SA in intestinal I/R injury is unclear. Thus, the present study aimed to investigate the protective effect of SA against intestinal I/R injury. Caco-2 cells were incubated with different doses of SA before oxygen-glucose deprivation/reoxygenation (OGD/R) induction. The viability of Caco-2 cells, the activity of lactate dehydrogenase (LDH), the production of pro-inflammatory cytokines and the levels of reactive oxygen species, superoxide dismutase and malondialdehyde were measured. Apoptosis was evaluated using a TUNEL assay and western blotting. Transepithelial electrical resistance and western blotting were performed to evaluate intestinal barrier function in Caco -2 cells. The present study revealed that pretreatment with SA significantly increased cell viability and reduced LDH release in Caco-2 cells subjected to OGD/R treatment. In addition, SA suppressed OGD/R-induced inflammatory responses by reducing pro-inflammatory cytokine levels. Furthermore, the levels of oxidative stress and apoptosis were ameliorated by SA. SA also alleviated the intestinal barrier disruption exhibited by Caco-2 cells after OGD/R injury. Overall, the present study revealed that SA may potentially protect Caco-2 cells from OGD/R injury, and that this effect may be attributed to its anti-inflammatory and anti-apoptotic activities, as well as its ability to protect the function of the intestinal barrier.

PMID:34 934437 | PMC:PMC8649867 | DOI:10.3892/etm.2021.10989

View on the web

Δεν υπάρχουν σχόλια:

Δημοσίευση σχολίου