A Hypothesis: Supplementation with Mushroom-Derived Active Compound Modulates Immunity and Increases Survival in Response to Influenza Virus (H1N1) Infection.

School of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250355, China.
Evidence-based Complementary and Alternative Medicine (Impact Factor: 1.72). 01/2011; 2011:252501. DOI: 10.1093/ecam/neq037
Source: PubMed

ABSTRACT We hypothesize that the mushroom-derived active compound may be a potential strategy for increasing survival in response to influenza virus (H1N1) infection through the stimulation of host innate immune response. The validity of the hypothesis can be tested by immune response to influenza infection as seen through survival percentage, virus clearance, weight loss, natural killer cell cytotoxicity, Tumor Necrosis Factor-α (TNF-α) and Interferon-gamma (IFN-γ) levels, lytic efficiency in the spleens of mice and inducible nitric oxide synthase mRNA expressions in RAW 264.7 murine macrophage cells. The hypothesis may improve people's quality of life, reduce the medical cost of our healthcare system and eliminate people's fears of influenza outbreak.

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    ABSTRACT: Brain ischemia-reperfusion (IR) triggers a complex series of biochemical events including inflammation. To test the neuroprotective efficacy of Cordyceps sinensis mycelium (CSM) in a rat model of focal cerebral IR, ischemic animals were treated with CSM. They were evaluated at 24 h after reperfusion for neurological deficit score. Furthermore, the mechanism of the anti-inflammatory potential of CSM in the regulation of nuclear factor kappaB, polymorphonuclear cells (PMN), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), adhesion molecule (ICAM-1), and cyclooxygenase-2 (COX-2) was determined by ELISA and immunohistochemistry. CSM significantly inhibited IR-induced up-regulation of NF-kappaB activation and the brain production of IL-1β, TNF-α, iNOS, ICAM-1, and COX-2. Moreover, CSM suppressed infiltration of PMN. The study demonstrates the neuroprotective potential of CSM inhibition through anti-inflammation in a rat model of ischemia-reperfusion.
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