LBP and diabetes mellitus: Mechanistically, LBP inhibited the advanced glycosylation end products (AGEs) formation and polyol and protein kinase C (PKC) pathway activation to reduce the generation of ROS; as well as inhibited the ERK1/2 phosphorylation, inhibitor of nuclear factor-κB α (IκBα) degradation, and nuclear translocation of NF-κB p65 to interrupt the downstream inflammatory cascade, ultimately improving DM-induced renal inflammation (72, 73, 75, 77, 78).