The anti-inflammatory effect of Lithospermum Erythrorhizon on lipopolysaccharide - induced inflammatory response in RAW 264.7 cells
| Autor: | Sun-Bok Choi, Joon-Yeon Shin, Jung-Hyun Lee, Kyoung-Chel Park, Seung-Hee Seo, Tae-Sin Gwak, Il-Joo Jo, Sung-Joo Park, Dong-Goo Kim, Guemsan Lee, Gi-Sang Bae, Ho-Joon Song |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
medicine.medical_specialty
biology Lipopolysaccharide medicine.drug_class p38 mitogen-activated protein kinases Interleukin Inflammation Pharmacology Lithospermum erythrorhizon biology.organism_classification Anti-inflammatory chemistry.chemical_compound Endocrinology chemistry Internal medicine medicine Tumor necrosis factor alpha medicine.symptom RAW 264.7 Cells |
| Zdroj: | The Korea Journal of Herbology. 28:67-73 |
| ISSN: | 1229-1765 |
| DOI: | 10.6116/kjh.2013.28.2.67 |
| Popis: | Objective ： Lithospermum Erythrorhizon (LE) has been used as an anti-bacterial and anti-inflammatory agent. However, it is unclear that LE aqueous extract could show the anti-inflammatory effects in RAW 264.7cells. The purpose of this study was to investigate the anti-inflammatory effect of aqueous extract from LE on lipopolysaccharide (LPS) - induced inflammatory response. Methods ： To measure out the cytotoxicity of LE, we performed the MTT assay. To evaluate the anti-inflammatory effects of LE, we examined the inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin, (IL)-1β and (IL)-6) on RAW 264.7 cells. We also examined molecular mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor-B (NF-κB) activation by western blot. Results ： Aqueous Extract from LE itself did not have any cytotoxic effect in RAW 264.7 cells. Aqueous extract from LE inhibited LPS-induced productions of inflammatory mediators such as NO, PGE2, and pro-inflammatory cytokines including TNF-α, IL-1β and IL-6 in RAW 264.7cells. In addition, LE inhibited the phosphorylation of p38 kinases (p38), c-Jun NH2-terminal kinase (JNK), and NF-κB activation in RAW 264.7 cells. Conclusion ： LE down-regulated LPS-induced production of inflammatory mediators through the inhibition of p38, JNK and NF-κB activation. Taken together, these results could provide the evidence for the anti-inflammatory effects of LE. Therefore, LE may be a novel target in the management of inflammation and help to support a potential strategy for prevention and therapy of inflammatory diseases. |
| Databáze: | OpenAIRE |
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