Objective To investigate the value of flexi-rigid thoracoscopy in pleural effusion of unknown causes and the correlation with CEA, TK1 and ADA. Methods The clinical data and results of CEA, TK1 and ADA of 25 patients were retrospective analyzed in our department from 2015 January to November 2015. These patients accepted the examination of flexi-rigid thoracoscopy with pleural effusion of unknown causes. Results In the 25 patients with pleural effusion of unknown causes, definite diagnosis was made in 22 cases (88.00 %), of which 9 cases were malignant pleural effusion (36.00 %), 11 cases were tuberculous pleural effusion (44.00 %), 2 cases were inflammatory pleural effusion (8.00 %), 3 cases were undetermined (12.00 %). The positive rate of TK1 and CEA in malignant group was significantly higher than that in the tuberculosis group and inflammatory group, the positive rate of ADA in the tuberculosis group was significantly higher than that in the malignant group and inflammatory group. Conclusion Flexi-rigid medical thoracoscopy examination is an effective and safe method for diagnosis of unexplained pleural effusion with high exact diagnosis rate, less trauma and less complication. Combination with CEA, TK1 and ADA are helpful to improve diagnostic rate of pleural effusion of unknown causes.

Isatis indigotica Fort. (Ban-Lan-Gen) is an herbal medicine prescribed for influenza treatment. However, its active components and mode of action remain mostly unknown. In the present study, erucic acid was isolated from Isatis indigotica Fort., and subsequently its underlying mechanism against influenza A virus (IAV) infection was investigated in vitro and in vivo. Our results demonstrated that erucic acid exhibited broad-spectrum antiviral activity against IAV resulting from reduction of viral polymerase transcription activity. Erucic acid was found to exert inhibitory effects on IAV or viral (v) RNA-induced pro-inflam-matory mediators as well as interferons (IFNs). The molecular mechanism by which erucic acid with antiviral and anti-inflammatory properties was attributed to inactivation of NF-kB and p38 MAPK signaling. Furthermore, the NF-kB and p38 MAPK inhibitory effect of erucic acid led to diminishing the transcriptional activity of interferon-stimulated gene factor 3 (ISGF-3), and thereby reducing IAV-triggered pro-inflammatory response amplification in IFN-β-sensitized cells. Additionally, IAV- or vRNA-triggered apoptosis of alveolar epithelial A549 cells was prevented by erucic acid. In vivo, erucic acid administration consistently displayed decreased lung viral load and viral antigens expression. Meanwhile, erucic acid markedly reduced CD8+cytotoxic T lymphocyte (CTL) recruitment, pro-apoptotic signaling, hyperactivity of multiple signaling pathways, and exacerbated immune inflammation in the lung, which resulted in decreased lung injury and mortality in mice with a mouse-adapted A/FM/1/47-MA(H1N1) strain infection. Our findings provided a mechanistic basis for the action of erucic acid against IAV-mediated inflammation and injury, suggesting that erucic acid may have a therapeutic potential in the treatment of influenza.