Vanillic acid alleviates lipopolysaccharides-induced endoplasmic reticulum stress and inflammation in human lung fibroblasts by `inhibiting MAPK and NF-κB pathways

Persistent endoplasmic reticulum stress promotes aberrant inflammation and induces cell death, is implicated in the pathogenesis of pneumonia. Vanillic acid exerts pharmacological activities, such as anti-inflammatory, antimicrobial, antioxidant effects. However, role vanillic pneumonia has not been elucidated yet. Human lung fibroblasts (WI-38 MRC-5) were incubated with different concentrations lipopolysaccharides to mimic model Lipopolysaccharides-treated then acid. Cell viability apoptosis detected by MTT assay flow cytometry, respectively. Quantitative real-time polymerase chain reaction enzyme-linked-immunosorbent serologic used measure levels inflammatory factors. Western blot was detect downstream pathway. Lipopolysaccharides induced decrease WI-38 MRC-5 whereas increased lipopolysaccharides-treated fibroblasts. Lipopolysaccharides-induced increase suppressed through up-regulation BCL2, down-regulation BCL2 associated X (BAX) cleaved caspase-3. reduced tumor necrosis factor-α (TNF-α), Interleukin 6 (IL-6), IL-1β Protein expression glucose-regulated protein 78 (GRP78), X-box binding 1 (XBP-1), activating transcription factor-6 (ATF-6), ATF-4, C/EBP homologous (CHOP) up-regulated while attenuated lipopolysaccharides-induced IκBα p-IκBα, p-p65, p-ERK, p-JNK exerted anti-inflammatory effect against human inhibiting mitogen-activated kinase nuclear factor kappa B pathways.