Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty-four rats were exposed intratracheally to 25 mg of locally produced Xinkang short-fiber chrysotile asbestos (98% of the fibers are less than 5 microns in length). In 1 to 3 d after instillation, the pathological changes in rat lungs demonstrated that the affection was mainly acute bronchio-alveolitis characterized by acute inflammatory exudation and injuries of the small airways and alveolar structural units. The four main manifestations of alveolitis induced by the chrysotile asbestos were of the neutrophilic, serous, alveolar macrophages and granulomatous varieties. Three types of pulmonary fibrosis developed gradually from 7 to 90 d following the exposure to the asbestos, i.e. the intraluminal, murally incorporated, and interstitial fibrosis. Findings showed the complete process from the acute inflammatory exudation and the damage to lung tissue, with the following repair and proliferation of injuried lung tissue and organization of exudate, to the final fibrosis and destruction of the lung. The results suggested that the persistent and irreversible damage to the epithelial cells of respiratory bronchioles and pneumocytes, and denudation and destruction of the basement membrane played an important role in the development of pulmonary fibrosis by forming a channel for the inflammatory exudates and fibroblasts migrating into the bronchioalveolar spaces. Therefore, the experimental results have proved that Xinkang chrysotile asbestos fibers less than 5 microns in length certainly have a fibrogenic effect.
Hua Xi Yi Ke Da Xue Xue Bao 1989 Sep
PMID:[Pathological study of bronchio-alveolitis induced by xinkang short-fiber chrysotile asbestos in rats]. 262 35

Diffusion capacity for carbon monoxide of the lung (DLCO) before-and-after exercise test and 5 routine pulmonary function tests were conducted in 16 patients with diffuse pulmonary fibrosis (DPF), 19 patients with interstitial pneumonia (IP), 17 patients with COPD, and 22 normal subjects. The data showed: in normal subjects the DLCO after exercise increased significantly compared with before (P < 0.001). But in DPF group the DLCO before exercise was below the normal range, and it went down further after exercise, the decreasing rate being 17.95% (P < 0.001). The DLCO in IP and COPD groups did not significantly change before and after the exercise. Two cases of interstitial pneumonia, who had a reduced DLCO after exercise, were followed up for 0.5-1.0 year, and both patients developed into DPF by that time. The results suggest that the DLCO measure before and after exercise test may have important value for DPF diagnosis, and a reduced DLCO after exercise test in IP patients may warn the development from IP into DPF.
Hua Xi Yi Ke Da Xue Xue Bao 1996 Jun
PMID:[Diagnostic value of exercise diffusion capacity test on diffuse pulmonary fibrosis]. 938 39

Pulmonary fibrosis, a progressive chronic disease with a high mortality rate, has limited treatment options. Currently, lung transplantation remains the only effective treatment. Here we report that a small RNA, HJT-sRNA-m7, from a Chinese herbal medicine Hong Jing Tian (HJT, RHODIOHAE CRENULATAE RADIX ET RHIZOMA, Rhodiola crenulata) can effectively reduce the expressions of fibrotic hallmark genes and proteins both in alveolar in vitro and in mouse lung tissues in vivo. We also discovered over one hundred oil-soluble chemicals from HJT decoctions, most of which are found in lipid extracts from other Chinese herbals decoctions, including Pu Gong Ying (PGY, TARAXACI HERBA, Taraxacum mongolicum), Chuan Xin Lian (CXL, changed to "ANDROGRAPHIS HERBA, Andrographis paniculata"), and Jin Yin Hua (JYH, lonicera japonica or Honeysuckle). We identified the active component in these decoctions as two forms of phosphocholines, PC (18:0/18:2) and PC (16:0/18:2). These PCs potentially could form liposomes with small RNAs to enter human alveolar and gastric cells. Our experimental results suggest an unprecendent lipid complex route through which botanic small RNA can enter human bodies. Our results provide an innovative treatment strategy for oral delivery of siRNAs as therapeutic medication.
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PMID:Plant-derived phosphocholine facilitates cellular uptake of anti-pulmonary fibrotic HJT-sRNA-m7. 2837 54

Mycobacterium tuberculosis (M.tb) infection in lung causes pulmonary fibrosis, which leads to the irreversible reduction of pulmonary function. Fibrotic protein connective tissue growth factor (CTGF) expression has been confirmed to play a crucial role in lung fibrosis. However, the underlying signal pathway and effect of M.tb on CTGF expression in human lung fibroblasts are unclear. Our results revaled that M.tb caused time- and concentration-dependent increases in CTGF expression in human lung fibroblasts. A mechanistic investigation revealed that M.tb induced CTGF expression through TLR2 but not TLR4. The promoter activity assay indicated that M.tb-induced CTGF activity was mainly controlled by the promoter region at -747 to -184 bp, which contained signal transducer and activator of transcription 3 and activator protein 1 (AP-1) binding sites. Moreover, curcumin (AP-1 inhibitor) restrained M.tb-induced CTGF expression. M.tb also induced increases in AP-1 luciferase activity and DNA binding activity of c-Jun and c-Fos on the CTGF promoter. Furthermore, the knockdown of c-Jun by small interfering RNA attenuated M.tb-induced CTGF expression and AP-1 luciferase activity. A JNK inhibitor (SP600125) and a JNK dominant-negative mutant suppressed M.tb-induced CTGF expression. We also discovered that M.tb could induce the phosphorylation of JNK and c-Jun. Furthermore, SP600125 inhibited M.tb-induced c-Jun phosphorylation and AP-1- luciferase activity. M.tb-induced fibronectin expression was inhibited by anti-CTGF antibody. These results demonstrate that M.tb is activated through TLR2 to induce JNK activation, further increasing the DNA binding activity of c-Jun and c-Fos and finally inducing CTGF expression and extracellular matrix production.-Lee, H.-S., Hua, H.-S., Wang, C.-H., Yu, M.-C., Chen, B.-C., Lin, C.-H. Mycobacterium tuberculosis induces connective tissue growth factor expression through the TLR2-JNK-AP-1 pathway in human lung fibroblasts.
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PMID:Mycobacterium tuberculosis induces connective tissue growth factor expression through the TLR2-JNK-AP-1 pathway in human lung fibroblasts. 3145 Oct 10