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Sesquiterpene Coumarins from Ferula sinkiangensis Act as Neuroinflammation Inhibitors

Yachao XingSchool of Traditional Chinese Materia Medica 49﹟, Shenyang Pharmaceutical University, Shenyang, ChinaNing LiSchool of Traditional Chinese Materia Medica 49﹟, Shenyang Pharmaceutical University, Shenyang, ChinaDi ZhouSchool of Traditional Chinese Materia Medica 49﹟, Shenyang Pharmaceutical University, Shenyang, ChinaGang ChenSchool of Traditional Chinese Materia Medica 49﹟, Shenyang Pharmaceutical University, Shenyang, ChinaKun JiaoCollege of Life and Health Sciences, Northeastern University, Shenyang, ChinaWenli WangSchool of Traditional Chinese Materia Medica 49﹟, Shenyang Pharmaceutical University, Shenyang, ChinaYing-Ying SiSchool of Traditional Chinese Materia Medica 49﹟, Shenyang Pharmaceutical University, Shenyang, ChinaYue HouCollege of Life and Health Sciences, Northeastern University, Shenyang, China
2016en
ABI

Annotatsiya

Neuroinflammation mediated by microglia cells plays a critical role in the development of Alzheimer′s disease. To identify novel natural neuroinflammation inhibitors, a bioactivity-guided phytochemical research was performed on the traditional Chinese medicine “Awei”, that exhibited a significant inhibitory effect on nitric oxide production in over-activated microglia cells. The research identified sixteen bioactive sesquiterpene coumarins (two new and fourteen known ones) in the effective extract of <i>Ferula sinkiangensis</i>. Further, the anti-neuroinflammatory activities in BV-2 microglial cells were evaluated by monitoring LPS-induced nitric oxide production. In conclusion, the major constituent, (3′<i>S</i>, 5′<i>S</i>, 8′<i>R</i>, 9′<i>S</i>, 10′<i>R</i>)-kellerin (1.5 %, w/w), should be responsible for the anti-neuroinflammatory effect exhibited by Awei. Furthermore, it might be a potential natural therapeutic agent for Alzheimer′s disease. The research indicated moreover, that its primary mechanism is the inhibition of mRNA expression of the inflammatory cytokines nitric oxide, tumor necrosis factor-α, cyclooxygenase-2, interleukin-6 and interleukin-1<i>β</i>.

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