Ginkgolide B Suppresses TLR4-Mediated Inflammatory Response by Inhibiting the Phosphorylation of JAK2/STAT3 and p38 MAPK in High Glucose-Treated HUVECs

<div>Ginkgolide B inhibits high glucose-induced increase in the association between PAFR and TLR4. HUVECs were treated with 0.6 mg/ml ginkgolide B for 1 h, and glucose was then added for another 8 h. Coimmunoprecipitation (Co-IP) was performed using an anti-TLR4 antibody or an anti-PAFR antibody. Rabbit IgG served as a nonimmune control. (a) PAFR expression was determined by immunoprecipitation with anti-TLR4 antibody. (b) TLR4 expression was determined by immunoprecipitation with anti-PAFR antibody. The input represents whole cell lysate. The data were obtained from three independent experiments.</div>

Oxidative Medicine and Cellular Longevity

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Figure 3: Ginkgolide B Suppresses TLR4-Mediated Inflammatory Response by Inhibiting the Phosphorylation of JAK2/STAT3 and p38 MAPK in High Glucose-Treated HUVECs 

Figure 3 | Ginkgolide B Suppresses TLR4-Mediated Inflammatory Response by Inhibiting the Phosphorylation of JAK2/STAT3 and p38 MAPK in High Glucose-Treated HUVECs 