Figure 2: CD36 participates in LPS-induced inflammation in pGMECs. | Scientific Reports

Figure 2: CD36 participates in LPS-induced inflammation in pGMECs.

From: CD36 regulates lipopolysaccharide-induced signaling pathways and mediates the internalization of Escherichia coli in cooperation with TLR4 in goat mammary gland epithelial cells

Figure 2

(A,B) Changes in CD36 and TLR4 mRNA levels are shown. Cells were pretreated with NC or si-CD36 for 24 h and then treated with LPS for 12 h. CD36 and TLR4 mRNA levels increased following the addition of various concentrations of LPS. (C) Bright field and fluorescence images of pGMECs infected with Ad-GFP (left, upper) and Ad-CD36 (left, lower) adenovirus for 24 h (MOI = 100). The changes in CD36 mRNA levels compared with the control group, Ad-GFP group, and Ad-CD36 group are shown. (D,E) CD36 and TLR4 mRNA changes in pGMECs pretreated with siRNA or adenovirus and then exposed to 10 μg/ml LPS for 12 h. (F) The variation in NF-κB mRNA levels following the manipulation of CD36 in pGMECs. NF-κB mRNA levels were influenced by knockdown (left) or overexpression (right) of CD36 in pGMECs, which were then stimulated with 10 μg/ml LPS. (G) MyD88 mRNA levels and TRAF6 protein levels were influenced by CD36 expression in LPS-stimulated pGMECs. The values are the mean ± SEM for three individuals. Quantitative PCR data were normalized to GAPDH, UXT, and MRPL39. All data are presented as the mean ± SEM from three experiments. *P < 0.05, **P < 0.01, ***P < 0.001, and not significant (NS).

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