Redox Biology
·
2024
·
IF 10.7
Ming-Yan Wang,Meng-Xu Yi,Xing-Yu Mo,Shan-Jie Wei,Yu Qiao,Zheng Zhang,Zhao-Liang Su,Hong-Yan Lu
Bronchopulmonary dysplasia (BPD) is a severe lung disease in preterm infants, the abnormal proliferate and differentiate ability of type II epithelial cells (AEC II) is the key to the pathological basis of BPD. Mechanisms regarding abnormal AEC II in BPD remain unclear. The present work investigated the role and mechanisms of invariant natural killer T (iNKT) cells in lung disorder in BPD using public datasets, clinical samples, a hyperoxia-induced BPD mouse model and AEC II-iNKT cells transwell co-culture system. Firstly, we found that the NKT cells development factor IL-15 increased over time in patients with BPD in public databases, and clinically collected peripheral blood NKT cells in patients with BPD were increased. Subsequently, the percentage of iNKT cells increased in hyperoxia group compared with normoxia group, with the highest at P7, accompanied by increased activation with abnormal lung development. The administration of anti-CD1d neutralizing antibody to inhibit iNKT cells could alleviate the abnormal lung development of hyperoxia group mice, while α-GalCer administration could aggravate lung injury in hyperoxia group mice, and adoptive transfer of iNKT cells could aggravate the abnormal lung development in hyperoxia group mice. In addition, to further verify the role of iNKT cells on AEC II, AEC II-iNKT cells co-culture system was established. The presence of iNKT cells could aggravate the abnormal expression of SP-C and T1α under hyperoxia. Meanwhile, RNA-seq analysis showed that ferroptosis-related genes were highly expressed in AEC II co-cultured with iNKT cells under hyperoxia. We further validated the effect of the presence of iNKT cells under hyperoxia environment on AEC II ferroptosis levels, suggested that iNKT cells promote AEC II ferroptosis under hyperoxia, accompanied by decreased expression of SP-C and T1α. Our study found that the recruitment of iNKT cells in the lung may be an important cause of alveolarization disorder in BPD.
研究领域:
免疫学
·
肺科学
·
儿科
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF MOLECULAR STRUCTURE
·
2023
·
IF 3.8
Nanhao Jin,Yuqi Liu,Xiaoming Liu,Yue Zhao,Han Chen,Xinying Wang,Yuebin Feng,Huilong Luo,Wei Li
Four MOFs with two identical structures were constructed by using 1,4-bis(4-pyridyl)-2,3-diaza-1,3-butadiene (4-bpd) and 1,3-dicarboxyadamantane (H 2 adc) as linkers, and Co 2+ , Ni 2+ as metal nodes by solvothermal method. Single-crystal X-ray diffraction revealed that complexes [Co 2 (adc) 2 (4-bpd)] n ( 1 ) and [Ni 2 (adc) 2 (4-bpd)] n ( 2 ) have the same two-dimensional molecular structure, while complexes [Ni(Hadc) 2 (H 2 O) 2 ] n ( 3 ) and [Co(Hadc) 2 (H 2 O) 2 ] n ( 4 ) exhibit identical one-dimensional chain-like molecular structures. The photo/electrocatalytic performances and thermal stability of four complexes were investigated. Introducing 4-bpd to form mixed-ligand complexes 1 and 2 enables the degradation of crystal violet (CV) dye in a Fenton-like system. Furthermore, there is an improvement in the oxygen evolution reaction (OER) catalytic performance among the MOFs of the same metal nodes. It is worth mentioning that in this study, Co-based MOFs showed better catalytic performance than Ni-based MOFs, which is mainly attributed to the distinctive electronic structure of Co 2+ and Ni 2+ d orbitals.
✓ 已验证
产品关联
DOI
高影响因子
JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
·
2024
·Vol. 75
·期 3
·
IF 2
Q Y Zhang,Y Feng,H Cai
Bronchopulmonary dysplasia (BPD) is a common serious complication of premature babies. No effective means control it. Hyperoxia damage is one of the important mechanisms of BPD. The reaserach confirmed pyroptosis existed in BPD. Dexmedetomidine is a new, high-specific α2 receptor agonist. Previous research foundation found that dexmedetomidine has a protective effect on BPD. To investigate how dexmedetomidine improves hyperoxic lung injury in neonatal mice by regulating pyroptosis. Neonatal rats were randomly divided into four groups: normal control group, hyperoxic injury group, air plus dexmedetomidine group, and hyperoxia plus dexmedetomidine group. After seven days the lungs of rats in each group were extracted, and the wet-to-dry weight ratio of the lung was measured. The lung injury in rats was observed using hematoxylin-eosin staining. Additionally, the expression and localization of nucleotide-binding oligomerization domain-like receptor thermal protein domain associated protein 3 (NLRP3), apoptosis-associated speck-like protein (ASC), and gasdermin D (GSDMD) proteins were examined in the lungs of rats using immunofluorescence staining. The mRNA levels of NLRP3, ASC, caspase-1, and interleukin 18 (IL-18) in the lungs of rats were determined using real-time PCR. Moreover, the protein levels of NLRP3, ASC, caspase-1/cleaved caspase-1, interleukin 1beta (IL-1β), IL-18, and tunor necrosis factor alpha (TNF-α) were detected in lungs of rats using Western blot. The extent of mitochondrial damage in lung tissues of each group was observed by transmission electron microscopy. The lung tissue injury of the neonatal rats was significantly improved in the hyperoxia plus dexmedetomidine group compared to the hyperoxic injury group. Furthermore, the expressions of pyroptosis-related proteins such as NLRP3, ASC, cleaved-caspase-1, and GSDMD were significantly decreased, along with the expressions of inflammatory factors in lung tissues. By inhibiting the NLRP3/caspase-1/GSDMD pyroptosis pathway, dexmedetomidine reduces the activation and release of inflammatory factors and provides a protective effect against hyperoxic lung injury in neonatal mice.
研究领域:
儿科
·
呼吸医学
·
药理学
·
分子生物学
·
免疫学
✓ 已验证
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）