Erythropoietin alleviates lung ischemia-reperfusion injury by activating the FGF23/FGFR4/ERK signaling pathway.

Background: The purpose of the present study was to investigate the effect of erythropoietin (EPO) on lung ischemia-reperfusion injury (LIRI). Methods: Sprague Dawley rats and BEAS-2B cells were employed to construct an ischemia-reperfusion (I/R)-induced model in vivo and in vitro, respectively. Afterward, I/R rats and tert-butyl hydroperoxide (TBHP)-induced cells were treated with different concentrations of EPO. Furthermore, 40 patients with LIRI and healthy controls were enrolled in the study. Results: It was observed that lung tissue damage, cell apoptosis and the expression of BAX and caspase-3 were higher in the LIRI model in vivo and in vitro than in the control group, nevertheless, the Bcl-2, FGF23 and FGFR4 expression level was lower than in the control group. EPO administration significantly reduced lung tissue damage and cell apoptosis while also up-regulating the expression of FGF23 and FGFR4. Rescue experiments indicated that EPO exerted a protective role associated with the FGF23/FGFR4/p-ERK1/2 signal pathway. Notably, the expression of serum EPO, FGF23, FGFR4 and Bcl-2 was decreased in patients with LIRI, while the expression of caspase-3 and BAX was higher. Conclusion: EPO could effectively improve LIRI, which might be related to the activation of the FGF23/FGFR4/p-ERK1/2 signaling pathway.

Zeaxanthin attenuates OVA-induced allergic asthma in mice by regulating the p38 MAPK/ß-catenin signaling pathway.

BACKGROUND: Asthma is a heterogeneous and complex chronic airway disease with a high incidence rate, characterized by chronic airway inflammation. Although the anti-inflammatory effect of zeaxanthin has been demonstrated in various disease models, its explicit role in allergic asthma remains elusive. METHODS: An allergic asthma model was established by ovalbumin (OVA) stimulation in BALB/c nude mice. The pathological examination, collagen deposition and expression of α-smooth muscle actin (α-SMA) in lung tissues were determined by hematoxylin and eosin (H&E), MASSON and immunofluorescence staining, respectively. Besides, the effect of zeaxanthin on inflammation and oxidative stress was assessed by the enzyme-linked immunosorbent assay (ELISA) and spectrophotometry measure. Moreover, the underlying mechanism was analyzed by detecting the expression of phosphorylated p38 (p-p38), p38, ß-catenin, p-c-Jun N-terminal kinase (p-JNK) and JNK with western blot assays. RESULTS: The distinct infiltration of inflammatory cells was observed in the OVA-induced asthma mice model with significantly increased concentrations of immunoglobulin E (IgE), interleukin-4 (IL-4), IL-5, IL-13 and eotaxin (p˂0.001), which were prominently reversed by zeaxanthin treatment (p˂0.001). In addition, zeaxanthin treatment decreased the OVA-induced collagen deposition and α-SMA expression. A similar inhibitory effect of zeaxanthin on the oxidative stress was also observed in the OVA-induced asthma mice model, as evidenced by the prominent decrease of malondialdehyde (MDA) concentration and the remarkable increase of superoxide dismutase (SOD), glutathione S transferase (GST) and Glutathione (GSH) concentrations (p˂0.001). Moreover, zeaxanthin introduction markedly reduced the relative expressions of p-p38/p38, ß-catenin and p-JNK/JNK in the OVA-induced asthma mice model (p˂0.001), indicating that zeaxanthin suppressed the p38 mitogen-activated protein kinase (p38 MAPK)/ß-catenin signaling pathway in the OVA-induced asthma mice model. CONCLUSIONS: Zeaxanthin attenuated OVA-induced allergic asthma in mice via modulating the p38 MAPK/ß-catenin signaling pathway.

[Clinical analysis of pulmonary embolism in a child with Mycoplasma pneumoniae pneumonia].

OBJECTIVE: To explore the essential points for diagnosis of pulmonary embolism in children with mycoplasma pneumonia. METHOD: Retrospective analysis of the clinical and laboratory data of a pediatric case who developed pulmonary embolism after mycoplasma pneumonia was performed for the key points for diagnosis. RESULT: A-six-year old boy was admitted with chief complaint of fever and cough for half a month, combined with chest pain and mild labored breath. Vital signs were stable. Breathing movement of the left side weakened and there was left lower lobe percussion dullness. Breath sound was found weakened in the left lung, and a few fine crackles were audible. The results of laboratory tests were as follows: mycoplasma antibody (IgM) 1:128, cold agglutinin test 1:1024, blood D dimer 14.81 mg/L; anticardiolipin antibody was positive; plasma protein C activity was 60% (normal range 70% - 130%). Pulmonary artery computed tomographic angiography revealed a mass opaque shadow in left lower lobe, the branch of left lower bronchial artery was partially obstructed. Echocardiography showed tricuspid valve mild regurgitation, estimated pulmonary pressure was 5.1 kPa. Single-photon emission computed tomography indicated that radioactivity distribution was apparently sparse in the dorsal segment, anterior basal segment, outer basal segment and inferior lingular segment of the left lung. The preliminary diagnosis on admission was mycoplasma pneumonia with pleural effusion, pulmonary embolism. Intravenous erythromycin combined with meropenem were administered. Anticoagulation therapy was initiated with low molecular weight heparin and then oral warfarin tablets. Pleural effusion disappeared soon, D dimer descended to 0.38 mg/L, and pulmonary artery pressure declined. After 3-month follow-up, anti-cardiolipin antibody was negative, plasma protein C activity recovered, and lung lesions were absorbed. CONCLUSION: When mycoplasma pneumonia is accompanied by chest pain or dyspnea and there are bloody pleural effusion, pulmonary hypertension, positive antiphospholipid antibody and elevated D dimer, pulmonary embolism should be considered. Diagnosis could be clarified by the result of pulmonary artery computed tomographic angiography.