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Active hexose correlated compound moderates lps‐induced gut injury in rats (LB576)
Author(s) -
Doursout MarieFrancoise,
Segal Graeme,
Ahn Stephanie,
Devakottai Sundar,
Liang Yangyan,
Wakame Koji,
Sundaresan Alamelu,
Kulkarni Anil
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.lb576
Subject(s) - inflammation , lipopolysaccharide , immune system , nitric oxide , pharmacology , blood pressure , medicine , oxidative stress , gut flora , immunology , chemistry , endocrinology
We hypothesize that Active Hexose Correlated Compound ( AHCC) , a fermented mushroom extract, restores immune function in lipopolysaccharide (LPS) induced inflammation in the gut, especially when endogenous nitric oxide (NO) signaling pathway is impaired. We identified the molecular mechanisms in the gut in rats subjected to LPS‐induced immune dysfunction, treated and non‐treated with AHCC, a potent promoter of immune support. Method: Six rats were instrumented under anesthesia to record mean arterial blood pressure (MAP) and heart rate (HR) and for drug administrations. Following recovery, conscious animals were pretreated with AHCC in drinking water (6%) prior to be subjected to LPS; 20 mg/kg; IV to induce inflammation. MAP and HR were continuously recorded for 3 hrs. following LPS administration. Simultaneously to hemodynamic measurements, blood samples were collected for NO and cytokines production. Animals were sacrificed at 3 hrs. and gut harvested to assess histology. Results and Conclusions: Ourpreliminary data have shown that AHCC induced reductions in LPS‐induced hypotension by 20% and gut edema by 30%. Cytokines e.g. TNF‐α, TGF β and IL‐1 were reduced by 40% in LPS rats pre‐treated with AHCC. Administration of AHCC prior to LPS challenge ameliorates LPS‐induced microvilli disruption in the gut. In summary, our data show that AHCC restored immune function in rats subjected to inflammation and specifically decreased excessive inflammation/oxidative stress in the gut. Grant Funding Source : None