Fig. 6: ER stress was activated by NETs, and ER stress inhibition alleviated NETs-induced damage in the intestinal epithelial cell monolayer. | Cell Death & Disease

Fig. 6: ER stress was activated by NETs, and ER stress inhibition alleviated NETs-induced damage in the intestinal epithelial cell monolayer.

From: Neutrophil extracellular traps impair intestinal barrier functions in sepsis by regulating TLR9-mediated endoplasmic reticulum stress pathway

Fig. 6

A Key molecules of ER stress were detected by western blotting in the Caco2 epithelial barrier model upon incubation with escalating doses of NETs. B The intensity of BIP and relative phospho-eIF2α expression were quantified using ImageJ software. C ROS production assessed by DCFH-DA and D cell viability tested by cell counting kit-8 in Caco2 monolayers after NETs (300 ng/ml) treatment with or without preincubation with 4-PBA or NAC. E TEER values were assessed after NETs (300 ng/ml) treatment with or without preincubation with 4-PBA or NAC. F The protein levels of key molecules of ER stress, caspase 3, and tight junction proteins in Caco2 epithelial barrier model after NETs (300 ng/ml) treatment with or without preincubation with 4-PBA. G The intensity was quantified using ImageJ software from three independent analyses. ER endoplasmic reticulum, NETs neutrophil extracellular traps, ROS reactive oxygen species, TEER transepithelial resistance. Data are expressed as the mean ± SD. *P < 0.05, **P < 0.01.

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