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Neuroinflammation and sickness induced by lipopolysaccharide in adult and aged mice are not mitigated by dietary broccoli (134.4)
Author(s) -
Townsend Brigitte,
Chen YungJu,
Jeffery Elisabeth,
Johnson Rodney
Publication year - 2014
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.28.1_supplement.134.4
Subject(s) - neuroinflammation , sulforaphane , lipopolysaccharide , hmox1 , sickness behavior , chemistry , medicine , endocrinology , heme oxygenase , inflammation , biochemistry , heme , enzyme
Aging is associated with chronic neuroinflammation and a heightened neuroinflammatory response during infection resulting in prolonged sickness. Dietary interventions to reduce neuroinflammation are therefore desirable. Broccoli contains glucoraphanin, which is converted to sulforaphane (SFN) during digestion. SFN activates antioxidants including heme oxygenase 1 (HMOX1) and NAD(P)H quinone oxidoreductase (NQO1) and inhibits production of interleukin‐1 (IL‐1β) by lipopolysaccharide (LPS)‐stimulated microglia. Therefore, we hypothesized that dietary broccoli would support an antioxidant response in the brain and inhibit LPS‐induced neuroinflammation and sickness. Adult and aged mice were fed control diet or control diet with 10% broccoli for 4 wk, and then injected i.p. with saline or LPS. After injection social behavior was assessed at 2, 4, 8, and 24 h; and HMOX1, NQO1, and IL‐1β mRNA were quantified in brain at 24 h. LPS reduced social behavior and increased HMOX1, NQO1, and IL‐1β in adult and aged mice (P<0.04); as expected, in aged mice IL‐1β was higher before LPS (P<0.004), tended to be higher after LPS (P=0.11), and restoration of normal behavior took longer (P<0.03). No significant effects of broccoli consumption were evident. Collectively, the results suggest that dietary broccoli does not affect neuroinflammation or sickness in adult or aged mice. Grant Funding Source : Supported by NIH R01AG016710