| Autor: |
Joung, Eun-Ji, Lee, Min-Kyeong, Lee, Minsup, Gwon, Misung, Shin, Taisun, Ryu, Heeyeon, Jeong, Hyeon Hak, Kim, Myeong-Jin, Van, Ji Yun, Kim, Jae-Il, Choi, Jinkyung, Jung, Won-Kyo, Kim, Hyeung-Rak, Lee, Bonggi |
| Předmět: |
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| Zdroj: |
Planta Medica; Jan2024, Vol. 90 Issue 1, p25-37, 13p |
| Abstrakt: |
This study aims to explore the anti-inflammatory mechanisms of sargachromenol in both RAW 264.7 cells and lipopolysaccharide (LPS)-treated mice, as previous reports have suggested that sargachromenol possesses anti-aging, anti-inflammatory, antioxidant, and neuroprotective properties. Although the precise mechanism behind its anti-inflammatory activity remains unclear, pretreatment with sargachromenol effectively reduced the production of nitric oxide, prostaglandin E2 , and interleukin (IL)-1 β in LPS-stimulated RAW 264.7 cells by inhibiting cyclooxygenase-2. Moreover, sargachromenol inhibited the activation of nuclear factor- κ B (NF- κ B) by preventing the degradation of the inhibitor of κ B- α (I κ B- α) and inhibiting protein kinase B (Akt) phosphorylation in LPS-stimulated cells. We also found that sargachromenol induced the production of heme oxygenase-1 (HO-1) by activating the nuclear transcription factor erythroid-2-related factor 2 (Nrf2). In LPS-treated mice, oral administration of sargachromenol effectively reduced the levels of IL-1 β , IL-6, and tumor necrosis factor- α (TNF- α) in the serum, suggesting its ability to suppress the production of inflammatory mediators by inhibiting the Akt/NF- κ B pathway and upregulating the Nrf2/HO-1 pathway. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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