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BackgroundChildren with severe adenoviral pneumonia (ADVP) have poor prognosis and high risk of mortality. We performed a meta-analysis to evaluate the association between pretreatment lactate dehydrogenase (LDH) and severity, postinfectious bronchiolitis obliterans (PIBO), and mortality in children with ADVP.MethodsRelevant observational studies were identified by search of PubMed, Embase, Web of Science, Wanfang, and CNKI databases from inception to August 3, 2022. A random effect model was used to pool the results by incorporating the potential between-study heterogeneity.ResultsOverall, 23 studies with 4,481 children with ADVP were included in this meta-analysis. Results of meta-analysis showed that children with severe ADVP had a significantly higher level of pretreatment LDH as compared to those with non-severe ADVP (standard mean difference [SMD]: 0.51, 95% confidence interval [CI]: 0.36 to 0.66, p < 0.001; I2 = 69%). Besides, pooled results also suggested that the pretreatment LDH was significantly higher in children who developed PIBO as compared to those who did not (SMD: 0.47, 95% CI: 0.09 to 0.84, p = 0.02, I2 = 80%). Finally, results of the meta-analysis also confirmed that a higher pretreatment LDH (>500 IU/L) was a risk factor of increased mortality during hospitalization (odds ratio: 3.10, 95% CI: 1.62 to 5.92, p < 0.001, I2 = 0%). Sensitivity analyses by excluding one dataset at a time showed consistent results.ConclusionHigh pretreatment LDH may be associated with disease severity, development of PIBO, and increased risk of mortality in children with ADVP.

The specific mechanism of gingerol in cerebral ischemia remains unknown. A neuroprotective function for miR‐210 in cerebral ischemia has been identified. The brain‐derived neurotrophic factor (BDNF)‐mediated signaling pathway protects against cerebral ischemic injury. This investigation aimed to determine whether gingerol plays a neuroprotective role in cerebral ischemia via the miR‐210/BDNF axis. N2a cells subjected to 10 h of hypoxia and 4 h of reoxygenation were treated with 5, 10, or 20 μmol/L gingerol. The levels of viability, apoptosis, and proteins in N2a cells were determined using MTT assays, flow cytometry, and western blotting, respectively. The binding relationship between BDNF and miR‐210 was studied using a dual luciferase reporter assay. The expression levels of miR‐210 and BDNF were determined using qPCR. Gingerol repressed the increase in apoptosis and decrease in viability observed in response to hypoxia/reoxygenation. Gingerol increased Bcl‐2, BDNF, and TrkB levels and reduced Bax and cleaved caspase 3 levels after hypoxia/reoxygenation. Gingerol evoked decreased expression of miR‐210. Inhibition of miR‐210 resulted in increased viability and reduced apoptosis along with increased levels of Bcl‐2, BDNF, and TrkB and reduced levels of Bax and cleaved caspase 3 after hypoxia/reoxygenation. Additionally, the miR‐210 mimic reversed changes induced by gingerol. The cotransfection of the miR‐210 mimic and wild type BDNF led to decreased luciferase activity. BDNF was negatively regulated by miR‐210. BDNF siRNA reversed these changes evoked by miR‐210 inhibition. Gingerol ameliorated hypoxia/reoxygenation‐stimulated neuronal damage by regulating the miR‐210/BDNF axis, indicating that gingerol is worthy of further application in cerebral ischemia therapy.

Pachymic acid (PA) plays a neuroprotective role during cerebral ischemia/reperfusion. However, the protective mechanisms of PA in cerebral ischemia/reperfusion have been not fully determined. This investigation aims to explore the neuroprotective role of PA in ischemia/reperfusion via miR‑155/NRF2/HO‑1 axis. The N2a cell line was induced by hypoxia/reoxygenation (H/R) to simulate the neuronal damage that occurs during cerebral ischemia/reperfusion. PA was used to treat H/R‑induced N2a cells. An MTT assay was used to determine cell viability. The protein levels of Bcl‑2, Bax, heme oxygenase‑1 (HO‑1) and nuclear factor E2‑related factor 2 (NRF2) were measured via Western blot analysis. The level of apoptosis of N2a cells was determined by flow cytometry. The expression levels of miR‑155 and NRF2 were quantified by real‑ti me PCR. PA treatment inhibits the increase in apoptosis induced by H/R and also enhances the viability of cells exposed to H/R. PA reverses the increased expression of miR‑155 caused by H/R. Furthermore, H/R does not change the expression of HO‑1 and NRF2, but PA upregulates the expressions of HO‑1 and NRF2. Additionally, NRF2 is the target of miR‑155. Inhibiting miR‑155 contributes to increased cell viability and decreased apoptosis via targeting the NRF2/HO‑1 pathway. Overall, PA prevents neuronal cell damage induced by hypoxia/reoxygenation via miR‑155/ NRF2/HO‑1 axis.