emodin has been researched along with Respiratory Distress Syndrome 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.
Respiratory Distress Syndrome: A syndrome characterized by progressive life-threatening RESPIRATORY INSUFFICIENCY in the absence of known LUNG DISEASES, usually following a systemic insult such as surgery or major TRAUMA.
| Excerpt | Relevance | Reference |
|---|---|---|
| "The aim of this experiment was to evaluate the efficacy of emodin on LPS-provoked alveolar hypercoagulation and excessive pulmonary inflammation in ARDS, and its potential mechanism." | 7.96 | Emodin improves alveolar hypercoagulation and inhibits pulmonary inflammation in LPS-provoked ARDS in mice via NF-κB inactivation. ( Cheng, Y; He, T; Li, S; Li, X; Liu, B; Shen, F; Wu, Y; Yang, G; Zheng, X, 2020) |
| "Inflammation is a defense and protective response to multiple harmful stimuli." | 5.43 | Emodin suppresses LPS-induced inflammation in RAW264.7 cells through a PPARγ-dependent pathway. ( Feng, SJ; Yu, HP; Zhang, W; Zhu, T, 2016) |
| "The aim of this experiment was to evaluate the efficacy of emodin on LPS-provoked alveolar hypercoagulation and excessive pulmonary inflammation in ARDS, and its potential mechanism." | 3.96 | Emodin improves alveolar hypercoagulation and inhibits pulmonary inflammation in LPS-provoked ARDS in mice via NF-κB inactivation. ( Cheng, Y; He, T; Li, S; Li, X; Liu, B; Shen, F; Wu, Y; Yang, G; Zheng, X, 2020) |
| "Inflammation is a defense and protective response to multiple harmful stimuli." | 1.43 | Emodin suppresses LPS-induced inflammation in RAW264.7 cells through a PPARγ-dependent pathway. ( Feng, SJ; Yu, HP; Zhang, W; Zhu, T, 2016) |
| 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 |
|---|---|
| Liu, B | 1 |
| Cheng, Y | 1 |
| Wu, Y | 1 |
| Zheng, X | 1 |
| Li, X | 1 |
| Yang, G | 1 |
| He, T | 1 |
| Li, S | 1 |
| Shen, F | 1 |
| Zhu, T | 1 |
| Zhang, W | 1 |
| Feng, SJ | 1 |
| Yu, HP | 1 |
2 other studies available for emodin and Respiratory Distress Syndrome
| Article | Year |
|---|---|
Emodin improves alveolar hypercoagulation and inhibits pulmonary inflammation in LPS-provoked ARDS in mice via NF-κB inactivation.
Topics: Animals; Emodin; Gene Expression Regulation; Inflammation; Lipopolysaccharides; Mice; NF-kappa B; Pu | 2020 |
Emodin suppresses LPS-induced inflammation in RAW264.7 cells through a PPARγ-dependent pathway.
Topics: Aconitum; Animals; Anti-Inflammatory Agents; Disease Models, Animal; Emodin; Humans; Inflammation; L | 2016 |