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(−)‐Nyasol, isolated from Anemarrhena asphodeloides suppresses neuroinflammatory response through the inhibition of I‐[kappa]B[alpha]degradation in LPS‐stimulated BV‐2 microglial cells
Author(s) -
Li Hua,
Lee Yu-ih,
Chang Hee Ryun,
Ryu Jae-Ha
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb437
Subject(s) - microglia , nitric oxide synthase , p38 mitogen activated protein kinases , nitric oxide , tumor necrosis factor alpha , nf κb , pharmacology , chemistry , mapk/erk pathway , neuroinflammation , prostaglandin e2 , lipopolysaccharide , kinase , inflammation , microbiology and biotechnology , immunology , biology , apoptosis , endocrinology , biochemistry
Activation of microglia has been associated with pathological hallmarks of several neurodegenerative diseases. The regulation of microglial activation by inhibiting the production of pro‐inflammatory molecules can be useful therapeutic approach against neurodegenerative disorders. Anemarrhena asphodeloides Bunge (Liliaceae) has been used as an anti‐pyretic, anti‐inflammatory and anti‐diabetic agent in traditional medicine in Korea, China and Japan. (−)‐Nyasol, a norlignan isolated from Anemarrhena asphodeloides , showed anti‐inflammatory potential in LPS‐activated BV‐2 microglial cells. (−)‐Nyasol suppressed the mRNA levels of tumor necrosis factor α (TNF‐α) and Interleukin 1β (IL‐1β) in activated microglial cells. It also inhibited the production of nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) by down‐regulation of inducible nitric oxide synthase (i‐NOS) and cyclooxygenase‐2 (COX‐2), respectively. These inhibitory effects were correlated with the suppression of LPS‐induced nuclear factor κB (NF‐κB) nuclear translocation through the inactivation of p38 mitogen‐activated protein kinase (MAPK). These results suggest that (−)‐nyasol can be a modulator in neuro‐inflammatory conditions induced by microglial activation.