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Type 1 diabetes mellitus (T1DM) is characterized by hyperglycemia manifesting as insufficient insulin. Toll-like receptor-4 (TLR4) has been implicated in diabetic osteoporosis. We established streptozotocin (STZ)-induced diabetic mouse model and examined the relevant osteoporosis factors in different experimental groups, the WT-CON group, WT-STZ group, KO-CON group and KO-STZ group, respectively. No obvious protection of TLR4 deletion was shown in mice with diabetes. There was no obvious difference in the body weight or blood glucose concentration between WT-STZ group and KO-STZ group. However, TLR4 deletion reduced the receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation. Furthermore, TLR4 knockout attenuated STZ-induced diabetic osteoporosis via inhibiting osteoblasts and pre-inflammation factors mediated by the NF-κB pathway. TLR4 deletion ameliorated STZ-induced diabetic osteoporosis in mice, and TLR4 may be used as a potential therapeutic target for the treatment of diabetic osteoporosis.

Diabetic nephropathy (DN) is a major cause of end-stage renal disease and one of the most severe diabetic complications. However, there is lack of effective treatments for DN and the underlying mechanisms of the renal injury remain unclear. In current study, we evaluated the effects of silibinin on DN and further explored the underlying mechanisms. We administrated silibinin to db/db mice for 10 weeks. Then we monitored the diabetic metabolic parameters, kidney function, oxidative stress and AKT signaling pathway in db/db mice. Administration of silibinin to db/db mice improved diabetic condition, as evidenced by the decrease of body weight, HbAc1level and serum insulin level in db/db mice. Silibinin prevented kidney injury and attenuated oxidative stress in db/db mice. Silibinin activated AKT signaling pathway and decreased the levels of p-GSK-3β, Bax and cleaved caspase-3. Silibinin ameliorates diabetic nephropathy by activating the AKT signaling pathway.