Our Western blot analysis showed that the expression levels of FN and CREB were significantly increased in the kidney tissue of HFD/STZ-induced diabetic rats and were efficiently inhibited by the posttreatment with BPS, suggesting that BPS inhibited the activation of p38 MAPK signaling pathway and attenuated the upregulated fibrosis process in this pathophysiological condition of DN (Figures 7(g) and 7(h) and Table 8). This evidence concerns the gene CREB1 and liver dysplastic nodule.