scholarly journals Ginkgo biloba Extract EGb761 Attenuates Bleomycin-Induced Experimental Pulmonary Fibrosis in Mice by Regulating the Balance of M1/M2 Macrophages and Nuclear Factor Kappa B (NF-κB)-Mediated Cellular Apoptosis

2020 ◽  
Vol 26 ◽  
Author(s):  
Ling Pan ◽  
Yuehong Lu ◽  
Zhanhua Li ◽  
Yuping Tan ◽  
Hongmei Yang ◽  
...  
2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Meng Li ◽  
Ya Li ◽  
JianSheng Li ◽  
Peng Zhao ◽  
Yunping Bai ◽  
...  

Objective. We aimed to evaluate the therapeutic effects and long-term effects of YKF and dissect the potential mechanisms. Materials and Methods. IPF rats were given YKF, prednisone, or pirfenidone, respectively, from day 1 to day 42, followed by a 28-day nonintervention interval through day 70. Forced vital capacity (FVC), histopathology, hydroxyproline (HYP) contents, lung coefficient, blood inflammatory cell populations, inflammatory cytokine levels of the lung tissues, and the expression of proteins involved in nuclear factor- (NF-) κB signaling pathway were evaluated on days 7, 14, 28, 42, and 70. Results. HYP contents, Ashcroft scores, lung coefficient, and pulmonary fibrosis blood cell populations increased significantly in IPF rats, while FVC declined. All the above-mentioned parameters were improved in treatment groups from day 7 up to day 70, especially in YKF group. The mRNA and protein expressions of tumor necrosis factor- (TNF-) α significantly decreased, while interferon- (IFN-) γ significantly increased, and phosphorylations of cytoplasm inhibitor of nuclear factor kappa-B kinase β (IKKβ), inhibitor of nuclear factor kappa-B α (IκBα), and NF-κB were obviously downregulated in YKF group from day 7 to day 70. Conclusion. YKF has beneficial protective and long-term effects on pulmonary fibrosis by anti-inflammatory response and alleviating fibrosis.


2020 ◽  
Vol 19 (1) ◽  
pp. 58-63
Author(s):  
Juan Tian ◽  
Tao Han ◽  
Minjuan Pan

Neonatal pneumonia is caused by inflammation mediated by lipopolysaccharide from gram negative bacteria. This type of pneumonia is characterized by inflammatory and apoptotic responses. In this study, we have examined the effect of friedelin on lipopolysaccharide-induced pneumonia and the role of nuclear factor kappa B in this process. Also, using the human pulmonary alveolar epithelial cells as a model we examined the effect of lipopolysaccharide on the cell apoptosis and its protection by friedelin. The results show that friedelin prevented lipopolysaccharide-induced acute pneumonia in neonatal rats and cellular apoptosis by suppressing the nuclear factor kappa B signaling pathway. In summary, this study shows that the friedelin exhibits a remarkable protective effect on lung tissues exposed to lipopolysaccharides.


2016 ◽  
Vol 25 (5) ◽  
pp. 397-399 ◽  
Author(s):  
Taku Fujimura ◽  
Yumi Kambayashi ◽  
Sadanori Furudate ◽  
Aya Kakizaki ◽  
Takanori Hidaka ◽  
...  

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