| First Author | Zheng D | Year | 2020 |
| Journal | Biomed Pharmacother | Volume | 129 |
| Pages | 110345 | PubMed ID | 32535385 |
| Mgi Jnum | J:302772 | Mgi Id | MGI:6510192 |
| Doi | 10.1016/j.biopha.2020.110345 | Citation | Zheng D, et al. (2020) Toll-like receptor 7 deficiency mitigates hyperoxia-induced acute lung injury in mice. Biomed Pharmacother 129:110345 |
| abstractText | INTRODUCTION: Toll-like receptor (TLR) 7 is an important mediator in inflammation. However, its role in hyperoxia-induced acute lung injury (HALI) remains to be elucidated. METHODS: C57BL/6 wild-type and C57BL/6 background TLR 7 deficiency mice were exposed to hyperoxia to stimulate HALI in airtight cages. Animals were sacrificed at 72 h post hyperoxia or room air exposure. Lung injury indicators were measured. Moreover, soluble epoxide hydrolase (sEH) activity was detected by a 14, 15-EET/DHET ELISA kit. Activation of activator protein (AP)-1 and nuclear factor kappa-B (NF-kappaB) was detected with enzyme linked immunosorbent assay kits. RESULTS: Our data revealed that pulmonary histological assay and wet to dry weight ratio, myeloperoxidase and malondialdehyde activity were reduced in TLR 7 deficiency mice compared with wild-type mice. Moreover, hyperoxia-caused elevation of sEH activity was reduced in TLR 7 deficiency mice. Transcription factors AP-1 activation was significantly inhibited in TLR 7 deficiency mice compared with wild-type mice. Similarly, the activation of NF-kappaB was reduced in TLR 7 deficiency mice. Tumor necrosis factor-alpha and interleukin-1beta, potent proinflammatory cytokines, were reduced in TLR 7 deficiency mice. CONCLUSION: TLR 7 deficiency is associated with inhibition of inflammation in HALI in mice. |
