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Chenguang Yao,Kanghong Hu,Caili Xi,Ni Li,Yanhong Wei 한국유전학회 2019 Genes & Genomics Vol.41 No.3
Background Enterovirus 71 (EV71) is the main pathogen of hand-foot-mouth disease (HFMD) and sometimes causes several neurological complications. However, the underlying mechanism of the host response to the virus infection remains unclear. Objective To reveal the cell-specific transcriptional response of cultured RD cells following infection with EV71, and better understand the molecular mechanisms of virus-host interactions. Methods The RD cells were infected with or without EV71 for 24 h, and then transcriptome sequencing and qRT-PCR were performed to analyze the transcriptome difference of functional genes. Results More than 15000 genes were identified in transcriptome sequencing. In comparison with uninfected RD cells, 329 DEGs were identified in cells infected with EV71. GO and KEGG pathway enrichment analysis showed that most of the DEGs were related to DNA binding, transcriptional regulation, immune response and inflammatory response, apoptosis inducing factors and enriched in JAK-STAT and MAPK signaling pathways. TXNIP (thioredoxin-interacting protein) gene was further demonstrated to play an important role participating in cellular apoptosis induced by EV71, and the apoptosis and death mediated by TXNIP during EV71 infection was triggered by viral 2A protease (2Apro), not 3C protease (3Cpro). Conclusion Our study demonstrated that RD cells have a significant response to EV71 infection, including immune response and apoptosis. 2Apro might be a key inducer relative to the cellular apoptosis and death mediated by TXNIP during EV71 infection. These data would contribute to preferably understand the process at the molecular level and provide theoretical foundation for diagnosis and treatment of EV71-related diseases.
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Jin Yuqin,Li Jialing,Ding Liang,Zhao Qing,Song Yuxian,Li Guifeng,Ji Jun,Ni Yanhong,Hu Qingang 대한독성 유전단백체 학회 2022 Molecular & cellular toxicology Vol.18 No.1
Background Oxidative stress is involved in the pathogenesis of various inflammatory diseases, such as periodontitis. When periodontitis occurs, reactive oxygen species (ROS) are overproduced and cannot be balanced by the antioxidant defense system, resulting in tissue damage. Madecassic acid (MA), an abundant triterpenoid in Centella asiatica (L.) Urban, has been used as a wound healing, antiinflammatory, and anticancer agent. Moreover, recent studies have shown that MA has an antioxidative effect, but the underlying mechanism remains unclear. Objective Here, we established an effective oxidative stress model induced by hydrogen peroxide (H 2 O 2 ) in human periodontal ligament fi broblasts (hPDLFs) to investigate the antioxidant and protective effects of MA against cell damage and its underlying mechanism of action. Results Pretreatment with MA inhibited cell apoptosis and promoted cell invasion and migration against oxidative injury induced by H 2 O 2 . In addition, MA was able to maintain mitochondrial membrane potential (ΔΨm) under oxidative stress. Notably, we found that MA restored redox balance by reducing intracellular ROS production. Furthermore, we investigated apoptosis-related proteins and found that the levels of anti-apoptosis markers Bcl-xL and Bcl-2 were remarkably upregulated, whereas that of the pro-apoptotic marker Bax was strikingly downregulated. Conclusions Collectively, these findings suggest that MA inhibits H 2 O 2 -induced oxidative stress and apoptosis of hPDLFs by reducing intracellular ROS production to maintain ΔΨm stability.
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