emodin has been researched along with Silicosis in 2 studies
Emodin: Purgative anthraquinone found in several plants, especially RHAMNUS PURSHIANA. It was formerly used as a laxative, but is now used mainly as a tool in toxicity studies.
emodin : A trihydroxyanthraquinone that is 9,10-anthraquinone which is substituted by hydroxy groups at positions 1, 3, and 8 and by a methyl group at position 6. It is present in the roots and barks of numerous plants (particularly rhubarb and buckthorn), moulds, and lichens. It is an active ingredient of various Chinese herbs.
Silicosis: A form of pneumoconiosis resulting from inhalation of dust containing crystalline form of SILICON DIOXIDE, usually in the form of quartz. Amorphous silica is relatively nontoxic.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Pulmonary silicosis is characterized by lung fibrosis, which leads to impairment of pulmonary function; the specific mechanism remains to be fully elucidated Emodin shows antifibrotic effects in several organs with fibrosis, however, it has not been investigated in pulmonary silicosis." | 7.83 | Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact. ( Chen, M; Dang, X; Liu, Y; Pang, Y; Ren, H; Shang, D; Wang, J; Yang, T, 2016) |
| "Pulmonary silicosis is characterized by lung fibrosis, which leads to impairment of pulmonary function; the specific mechanism remains to be fully elucidated Emodin shows antifibrotic effects in several organs with fibrosis, however, it has not been investigated in pulmonary silicosis." | 3.83 | Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact. ( Chen, M; Dang, X; Liu, Y; Pang, Y; Ren, H; Shang, D; Wang, J; Yang, T, 2016) |
| "Silicosis is a fatal pulmonary disease caused by the inhalation of silica dust, and characterized by inflammation and fibrosis of the lung, with no effective treatment to date." | 1.62 | Emodin attenuates silica-induced lung injury by inhibition of inflammation, apoptosis and epithelial-mesenchymal transition. ( Jia, Q; Lavin, MF; Li, C; Nie, X; Pang, X; Peng, C; Shao, H; Shao, L; Xia, Q; Yan, H; Yeo, AJ; Yu, G, 2021) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 1 (50.00) | 24.3611 |
| 2020's | 1 (50.00) | 2.80 |
| Authors | Studies |
|---|---|
| Pang, X | 1 |
| Shao, L | 1 |
| Nie, X | 1 |
| Yan, H | 1 |
| Li, C | 1 |
| Yeo, AJ | 1 |
| Lavin, MF | 1 |
| Xia, Q | 1 |
| Shao, H | 1 |
| Yu, G | 1 |
| Jia, Q | 1 |
| Peng, C | 1 |
| Yang, T | 1 |
| Wang, J | 1 |
| Pang, Y | 1 |
| Dang, X | 1 |
| Ren, H | 1 |
| Liu, Y | 1 |
| Chen, M | 1 |
| Shang, D | 1 |
2 other studies available for emodin and Silicosis
| Article | Year |
|---|---|
Emodin attenuates silica-induced lung injury by inhibition of inflammation, apoptosis and epithelial-mesenchymal transition.
Topics: A549 Cells; Acute Lung Injury; Animals; Anti-Inflammatory Agents; Apoptosis; Apoptosis Regulatory Pr | 2021 |
Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact.
Topics: Actins; Animals; Bronchoalveolar Lavage Fluid; Collagen Type I; Disease Models, Animal; Emodin; Enzy | 2016 |