Neonatal acute respiratory distress syndrome (NARDS) is a potentially fatal condition. This study investigates the role of miR-618 in NARDS pathogenesis and prognosis to explore a novel biomarker for disease monitoring. 110 NARDS patients and 90 healthy controls were enrolled. Serum miR-618 levels were measured using qRT-PCR. ROC curve, Spearman rank correlation, and Kaplan-Meier curves were used to estimate clinical significance. An LPS-induced A549 cell injury model was established to investigate the biological functions of miR-618. Cell viability, apoptosis, and inflammatory cytokine production were assessed. Target prediction and dual-luciferase reporter assay were employed. Serum miR-618 was elevated in NARDS patients and demonstrated good diagnostic performance. miR-618 positively correlated with disease severity indicators including SNAPPE-II score, oxygenation index, and NICU stay duration. High miR-618 expression was associated with lower 30-day survival. In vitro, miR-618 inhibition restored LPS-induced loss of cell viability, reduced apoptosis, ROS and MDA levels, and decreased TNF-α, IL-1β, and IL-6 secretion, while miR-618 upregulation exacerbated these effects. BCL2 overexpression reversed the detrimental effects induced by miR-618 overexpression. BCL2 was validated as a direct target of miR-618, and BCL2 silencing reversed the protective effects of miR-618 inhibition. miR-618 was enhanced in NARDS. miR-618 was related to disease severity and unfavorable prognosis. In vitro, miR-618 promoted inflammatory injury and apoptosis in LPS-induced A549 cells, at least partly through suppression of BCL2. These findings identify the miR-618/BCL2 axis as a candidate molecular pathway for further investigation in NARDS. Not applicable.
HBsAg loss remains a major challenge in chronic hepatitis B (CHB). This study aimed to characterize the dynamic changes in NK cell phenotypes, receptor expression, and cytokine profiles during pegylated interferon-α (PEG-IFNα) and nucleos(t)ide analogs (NAs) combination therapy and their association with clinical outcomes. Twenty-seven CHB patients receiving PEG-IFNα and NAs combination therapy were stratified into on-treatment HBsAg loss group (HBsAg < 0.05 IU/mL, n = 10) and non-HBsAg loss group (n = 17) at week 48. Flow cytometry assessed NK cell subsets (CD56bright, CD56dim) and receptor expression (NKG2D, NKp30, NKp46, KIR, NKG2A, TIM3). Serum cytokines (IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-10) were measured by ELISA. Correlations of virological markers with NK cell subsets/receptors or cytokines were analyzed. PEG-IFNα and NAs combination therapy expanded CD56bright NK cells while reducing CD56dim subsets in both on-treatment HBsAg loss and non-HBsAg loss groups. In the on-treatment HBsAg loss group, persistent KIR upregulation was observed in CD56bright NK cells, whereas CD56dim NK cells maintained elevated NKG2A expression. Cytokine analysis showed that the on-treatment HBsAg loss group exhibited significantly lower serum levels of pro-inflammatory cytokines (IFN-γ, TNF-α, IL-6, and IL-2), while maintaining higher levels of the anti-inflammatory cytokine IL-10. Correlation analysis revealed significant inverse correlations between HBsAg and CD56bright NK cell proportion/ receptor expression, whereas HBsAg correlated positively with CD56dim NK cell frequency in on-treatment HBsAg loss group. Moreover, HBsAg was positively correlated with pro-inflammatory cytokine levels in both treatment groups. PEG-IFNα and NAs combination therapy is associated with on-treatment HBsAg loss at week 48, potentially through optimizing cytokine responses, regulating NK cell balance (CD56bright/CD56dim) and related receptors. Study limitations include the single-center design and moderate sample size. MR-53-26-076931 Date of registration: 31 August 2026. Full name of the registry in the national medical research registration information system:Prediction of clinical curative effect of pegylated interferon a individualized intermittent treatment of nucleoside (acid) in patients with hepatitis B.
Osteoarthritis (OA) is a debilitating degenerative joint disorder characterized by progressive cartilage destruction and chronic inflammation, with no curative therapies available. To investigate the clinical significance and functional mechanism of miR-1287-5p in knee OA. A total of 130 primary knee OA patients and 100 age- and sex-matched healthy controls were enrolled. Serum miR-1287-5p levels were detected by RT-qPCR, and their correlations with clinical parameters were analyzed. In vitro OA model was established by stimulating human chondrocytes with IL-1β. Dual-luciferase reporter assay and RNA immunoprecipitation were performed to verify the target relationship between miR-1287-5p and PIK3R3. Rescue experiments were conducted to confirm the functional axis. Serum miR-1287-5p was markedly upregulated in OA patients, and its expression was positively correlated with disease severity, pain scores, cartilage degradation markers, and pro-inflammatory cytokines. ROC analyses demonstrate that serum miR‑1287‑5p shows promising diagnostic potential for distinguishing OA patients from healthy subjects and for discriminating advanced‑stage from early‑stage knee OA, based on our single‑centre observational cohort. Mechanistically, miR-1287-5p directly targeted and negatively regulated PIK3R3 expression in chondrocytes. Inhibition of miR-1287-5p relieved IL-1β-evoked cellular dysfunction, aberrant apoptosis and excessive secretion of matrix catabolic enzymes plus pro-inflammatory factors, and these mitigating effects were offset the knockdown of PIK3R3. Serum miR-1287-5p serves as a promising non-invasive biomarker for OA diagnosis and severity assessment. miR-1287-5p promotes chondrocyte injury and inflammation via targeting PIK3R3.
