The inhibition of enterovirus 71 induced apoptosis by Durvillaea antarctica through P53 and STAT1 signaling pathway

Author(s):  
Tiantian Xu ◽  
Yinghua Li ◽  
Hua‐lian Wu ◽  
Haiyang Chen ◽  
Houbo Wu ◽  
...  

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xu Gao ◽  
Jingya Dai ◽  
Guifang Li ◽  
Xinya Dai

Abstract Objective In this work, we investigated the effects of gambogic acid (GA) on lipopolysaccharide (LPS)-induced apoptosis and inflammation in a cell model of neonatal pneumonia. Method Human WI-38 cells were maintained in vitro and incubated with various concentrations of GA to examine WI-38 survival. GA-preincubated WI-38 cells were then treated with LPS to investigate the protective effects of GA on LPS-induced death, apoptosis and inflammation. Western blot assay was utilized to analyze the effect of GA on tropomyosin receptor kinase A (TrkA) signaling pathway in LPS-treated WI-38 cells. In addition, human AKT serine/threonine kinase 1 (Akt) gene was knocked down in WI-38 cells to further investigate the associated genetic mechanisms of GA in protecting LPS-induced inflammation and apoptosis. Results Pre-incubating WI-38 cells with low and medium concentrations GA protected LPS-induced cell death, apoptosis and inflammatory protein productions of IL-6 and MCP-1. Using western blot assay, it was demonstrated that GA promoted TrkA phosphorylation and Akt activation in LPS-treated WI-38 cells. Knocking down Akt gene in WI-38 cells showed that GA-associated protections against LPS-induced apoptosis and inflammation were significantly reduced. Conclusions GA protected LPS-induced apoptosis and inflammation, possibly through the activations of TrkA and Akt signaling pathway. This work may broaden our understanding on the molecular mechanisms of human neonatal pneumonia.





2002 ◽  
Vol 199 (1-2) ◽  
pp. 39-43 ◽  
Author(s):  
Tamaki Mikami ◽  
Tsutomu Takahashi ◽  
Akira Ishida ◽  
Yoshihiro Minamiya ◽  
Hiroyuki Ida ◽  
...  


Peptides ◽  
2014 ◽  
Vol 52 ◽  
pp. 23-28 ◽  
Author(s):  
Jianhua Zhu ◽  
Chenghong Zheng ◽  
Jie Chen ◽  
Jing Luo ◽  
Bintao Su ◽  
...  


2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Yan-Fang Xian ◽  
Zhi-Xiu Lin ◽  
Qing-Qiu Mao ◽  
Jian-Nan Chen ◽  
Zi-Ren Su ◽  
...  

The neurotoxicity of amyloid-β(Aβ) has been implicated as a critical cause of Alzheimer’s disease. Isorhynchophylline (IRN), an oxindole alkaloid isolated fromUncaria rhynchophylla,exerts neuroprotective effect againstAβ25–35-induced neurotoxicityin vitro. However, the exact mechanism for its neuroprotective effect is not well understood. The present study aimed to investigate the molecular mechanisms underlying the protective action of IRN againstAβ25–35-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Pretreatment with IRN significantly increased the cell viability, inhibited the release of lactate dehydrogenase and the extent of DNA fragmentation inAβ25–35-treated cells. IRN treatment was able to enhance the protein levels of phosphorylated Akt (p-Akt) and glycogen synthase kinase-3β(p-GSK-3β). Lithium chloride blockedAβ25–35-induced cellular apoptosis in a similar manner as IRN, suggesting that GSK-3βinhibition was involved in neuroprotective action of IRN. Pretreatment with LY294002 completely abolished the protective effects of IRN. Furthermore, IRN reversedAβ25–35-induced attenuation in the level of phosphorylated cyclic AMP response element binding protein (p-CREB) and the effect of IRN could be blocked by the PI3K inhibitor. These experimental findings unambiguously suggested that the protective effect of IRN againstAβ25–35-induced apoptosis in PC12 cells was associated with the enhancement of p-CREB expression via PI3K/Akt/GSK-3βsignaling pathway.



2002 ◽  
Vol 277 (21) ◽  
pp. 18383-18389 ◽  
Author(s):  
Margaret M. Mc Gee ◽  
Giuseppe Campiani ◽  
Anna Ramunno ◽  
Vito Nacci ◽  
Mark Lawler ◽  
...  


Author(s):  
Jianjian Zhuang ◽  
Yange Liu ◽  
Qingxia Yuan ◽  
Junsong Liu ◽  
Yan Liu ◽  
...  


2017 ◽  
Vol 95 ◽  
pp. 1631-1635 ◽  
Author(s):  
Dongwei Wang ◽  
Ping Chen ◽  
Lei Chen ◽  
Fanrong Zeng ◽  
Rongjia Zang ◽  
...  


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