Crotalaria ferruginea extract attenuates lipopolysaccharide-induced acute lung injury in mice by inhibiting MAPK/NF-κB signaling pathways

Objective: To evaluate the anti-inflammatory activity of Crotalaria ferruginea extract (CFE) and its mechanism. Methods: An intratracheal lipopolysaccharide (LPS) instillation-induced acute lung injury (ALI) model was used to study the anti-inflammatory activity of CFE in vivo. The LPS-induced shock model was used to analyze the effect of CFE on survival. LPS-stimulated RAW264.7 cell model was used to investigate the anti-inflammatory activity of CFE in vitro and the effects on mitogen-Activated protein kinase (MAPK) or nuclear factor-κB (NF-κB) signaling pathways. Results: CFE administration decreased the number of inflammatory cells, reduced the levels of tumor necrosis factor-α (TNF-A), monocyte chemotactic protein-1 (MCP-1), interleukin-6 (IL-6), and interferon-γ, and diminished protein content in the bronchoalveolar lavage fluid of mice. CFE also reduced lung wet-To-dry weight ratio, myeloperoxidase, and lung tissue pathological injury. CFE pre-Administration improved the survival rate of mice challenged with a lethal dose of LPS. CFE reduced LPS-Activated RAW264.7 cells to produce nitric oxide, TNF-α, MCP-1, and IL-6. Furthermore, CFE inhibited nuclear translocation and phosphorylation of NF-κB P65, extracellular signal-regulated kinase, c-Jun N-Terminal kinases, and P38 MAPKs. Conclusions: CFE exhibits potent anti-inflammatory activity in LPS-induced ALI mice, LPS-shock mice, and RAW264.7 cells, and its mechanism may be associated with the inhibition of NF-κB and MAPK signaling pathways. Crotalaria ferruginea may be a useful therapeutic drug for the treatment of ALI and other respiratory inflammations.

Crotalaria ferruginea extract attenuates lipopolysaccharide-induced acute lung injury in mice by inhibiting MAPK/NF-κB signaling pathways

Objective: To evaluate the anti-inflammatory activity of Crotalaria ferruginea extract (CFE) and its mechanism. Methods: An intratracheal lipopolysaccharide (LPS) instillation-induced acute lung injury (ALI) model was used to study the anti-inflammatory activity of CFE in vivo. The LPS-induced shock model was used to analyze the effect of CFE on survival. LPS-stimulated RAW264.7 cell model was used to investigate the anti-inflammatory activity of CFE in vitro and the effects on mitogen-Activated protein kinase (MAPK) or nuclear factor-κB (NF-κB) signaling pathways. Results: CFE administration decreased the number of inflammatory cells, reduced the levels of tumor necrosis factor-α (TNF-A), monocyte chemotactic protein-1 (MCP-1), interleukin-6 (IL-6), and interferon-γ, and diminished protein content in the bronchoalveolar lavage fluid of mice. CFE also reduced lung wet-To-dry weight ratio, myeloperoxidase, and lung tissue pathological injury. CFE pre-Administration improved the survival rate of mice challenged with a lethal dose of LPS. CFE reduced LPS-Activated RAW264.7 cells to produce nitric oxide, TNF-α, MCP-1, and IL-6. Furthermore, CFE inhibited nuclear translocation and phosphorylation of NF-κB P65, extracellular signal-regulated kinase, c-Jun N-Terminal kinases, and P38 MAPKs. Conclusions: CFE exhibits potent anti-inflammatory activity in LPS-induced ALI mice, LPS-shock mice, and RAW264.7 cells, and its mechanism may be associated with the inhibition of NF-κB and MAPK signaling pathways. Crotalaria ferruginea may be a useful therapeutic drug for the treatment of ALI and other respiratory inflammations.

Study on the relationship between the polymorphism of p53 gene intron 7 and non-small cell lung cancer (NSCLC) and p53 mutation in NSCLC tissues / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the relationship between p53 gene intron 7 polymorphism and non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>One hundred and five patients with NSCLC and 100 controls were selected with case-control analysis. Polymerase chain reaction (PCR), Apa I restriction enzyme digestion and agarose gel electrophoretic separation were used to identify genotypes of p53 intron 7 in peripheral blood. Then, NSCLC biopsy tissues (n=64) and NSCLC paraffin-embedded tissues (n=40) were selected for mutation analysis. PCR products of p53 exons 5-8 were sequenced on an automated sequencer following the identification of intron 7 genotypes as previously described.</p><p><b>RESULTS</b>In NSCLC patients, the homozygote positive for ApaI site in p53 intron 7 was 23.8%, the homozygote negative was 12.34%, and the heterozygote was 63.8%. Whereas in control group, the homozygote positive, the homozygote negative and the heterozygote were 44.0%, 11.0% and 45.0%, respectively (P<0.01). In the second part, mutation rate of p53 exons 5-8 was 20.0%, 50.0% and 52.9% in samples with ApaI positive, negative and heterozygotes, respectively (P<0.05).</p><p><b>CONCLUSION</b>p53 intron 7 ApaI polymorphism may be associated with human NSCLC.</p>

Medical thoracoscopy in the diagnosis of complicate pleural effusion / 中南大学学报(医学版)

OBJECTIVE@#To evaluate the role of medical thoracoscopy in the diagnosis of the pleural effusion of unknown etiology.@*METHODS@#The results of 36 patients with the pleural disease of unknown etiology diagnosed by medical thoracoscopy were retrospectively analyzed, including the pathologic results and the complications.@*RESULTS@#Among the 36 patients, 35 were determined with positive rate of 97.2%, and no serious complications was found.@*CONCLUSION@#Medical thoracoscopy is an important method of diagnosing complicate pleural effusion, and has high positive rate. It is a simple operation, with no serious complication, and fast recovery.

Effect of ginsenoside Rh2 on immunocompetence of alveolar macrophages in patients with non-small cell lung cancer / 中南大学学报(医学版)

OBJECTIVE@#To explore the effect of ginsenoside Rh2 (G-Rh2) on the excretion of cytotoxin-effecting molecule of alveolar macrophages (AM) in patients with non-small cell lung cancer (NSCLC).@*METHODS@#The concentration of tumor necrosis factor (TNF-alpha) and NO in the bronchoalveolar lavage fluid (BALF) and the cultured supernatants of AM in 35 patients with NSCLC were measured by ELISA and enzyme method,and levels of TNF-alpha and NO in the cultured supernatants of AM after being cultivated with IFN-alpha, G-Rh2, and IFN-alpha+G-Rh2 were measured by the same method.@*RESULTS@#AM in all the non-small cell lung cancer patients produced TNF-alpha and NO. The activity of TNF-alpha and NO was lower in the BALF and in the cultured supernatants of AM of the tumor-bearing lungs than that of the non-tumor-bearing lungs. The concentrations of TNF-alpha and NO in the cultured supernatants of AM cultivated with G-Rh2 were higher than those in the control (P0.05). The concentrations of TNF-alpha and NO in the cultured supernatants of AM cultivated with both G-Rh2 and IFNalpha were obviously higher than those stimulated with IFNalpha or G-Rh2 (P<0.01) alone.@*CONCLUSION@#G-Rh2 can enhance the excretion of cytotoxin-effecting molecules of AM in patients with NSCLC. The changes are more distinctive when G-Rh2 and IFNalpha have coordinated action.