http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-20200022193-A
Outgoing Links
| Predicate | Object |
|---|---|
| assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_2b4be2300a741a69aa1b8bb47a88899f |
| classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-7105 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K39-39533 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-4985 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-519 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P11-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K48-00 |
| classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K48-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K39-395 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P11-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-519 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-4985 |
| filingDate | 2018-08-22-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_c99c357bd3e5d3d411f1fcce93ae38ef http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_c624c302fe7e64955bb72943bd76c111 http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_dc947f91e5d23d5accb79a69628806bd |
| publicationDate | 2020-03-03-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber | KR-20200022193-A |
| titleOfInvention | Pharmaceutical composition for preventing or treating tuberculous pleural fibrosis |
| abstract | Tuberculous pleurisy often causes pleural fibrosis, which causes respiratory failure. NOX (NADPH oxidase) enzyme provides hemostasis and host defense in the lungs. However, the role of NOX4 signaling in tuberculous pleurisy is unknown. We have investigated the role of NOX4 signaling in tuberculous pleural fibrosis using in vitro pleural mesothelial cell experiments and BCG pleural infected mouse model. The results suggest that heat-killing mycobacterium tuberculosis induces NOX4-ROS production and epithelial mesenchymal migration in pleural mesothelial cells. TLR4 inhibitors, TAK-242 and rozatan, reduced NOX4-ROS production and subsequent fibrosis. SiRNA NOX4 pretreatment in cultured pleural mesothelial cells inhibited heat-killed Mycobacterium tuberculosis-induced collagen-1 synthesis and epithelial mesenchymal migration. NOX4 mediates heat treatment killing Mycobacterium tuberculosis-induced epithelial mesenchymal migration and intracellular reactive oxygen species generation through activation of ERK signaling. In the BCG induced pleurisy model, the BCG + SiNOX4 group (SiNOX4 IV post-BCG) reduced inflammatory pleural cell recruitment, inflammatory cytokine excretion and mesothelial fibrosis compared to the BCG + SiCon group (SiCon IV post-BCG). These results indicate that NOX4-ERK-ROS regulates heat-killed Mycobacterium tuberculosis-induced pleural fibrosis via TLR4 and AT1R. NOX4 may be a new therapeutic target in tuberculous pleural fibrosis. |
| isCitedBy | http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2023144742-A1 |
| priorityDate | 2018-08-22-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 464.