| First Author | Cao Y | Year | 2021 |
| Journal | Biochem Biophys Res Commun | Volume | 546 |
| Pages | 185-191 | PubMed ID | 33601314 |
| Mgi Jnum | J:305562 | Mgi Id | MGI:6706012 |
| Doi | 10.1016/j.bbrc.2021.01.102 | Citation | Cao Y, et al. (2021) TLR4 knockout ameliorates streptozotocin-induced osteoporosis in a mouse model of diabetes. Biochem Biophys Res Commun 546:185-191 |
| abstractText | 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-kappaB ligand (RANKL)-induced osteoclast differentiation. Furthermore, TLR4 knockout attenuated STZ-induced diabetic osteoporosis via inhibiting osteoblasts and pre-inflammation factors mediated by the NF-kappaB 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. |
