Bigelovii A Protects against Lipopolysaccharide-Induced Acute Lung Injury by Blocking NF-κB and CCAAT/Enhancer-Binding Protein δ Pathways

Figure 9

Effect of Bigelovii A on p38 MAPK/ERK1/2—C/EBPδ signaling pathway during LPS-induced inflammation in MH-S cells. (a) and (b) MH-S cells were pretreated with or without 10 μM of Bigelovii A for 1 h, followed by treatment with PBS or 100 ng/mL of LPS for 15 min, and total proteins were isolated. Western blot was performed by using antibodies against p-p38, p38, p-p44/42, p44/42, and GAPDH, respectively. (c) MH-S cells were transiently transfected with total of 0.5 μg indicated plasmids. 48 h after transfection, the cells were pretreated with or without 10 μM of Bigelovii A for 1 h, followed by treatment with PBS or 100 ng/mL of LPS. 4 h later, the cells were lysed, and luciferase activity was measured. Luminometer values were normalized for expression from a cotransfected pRL-TK gene and negative control sequentially. Results are reflected by means ± SEM (). and indicated statistically significant difference, and 0.01, respectively. Negative control: cells treated by Vehicle plus PBS. Positive control: cells receiving LPS plus Vehicle treatment.

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