アルコール濫用による細胞・組織防御システムの破綻機構

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1. It was clarified that ethanol regulates cell survival system via induction of IAP by NF-kappaB activation and activation of Akt.2. In the nonalcoholic fatty liver disease murine model, acute ethanol treatment caused no proinflammatory response via NF-kappaB, suggesting that inflammatory disturbance occurs in fatty liver disease.3. Polyunsaturated fatty acids caused sever inflammation in fatty liver. Then polyunsaturated fatty acid induced IL-10 release in hepatocytes, whichi may induce Kupffer cell activation.4. We established alcohol-related sudden death model. In this model, TLR4 signaling pathway did not play an important role in cause of death.5. In brain contusion model, prior ethanol injection promotes brain edema after traumatic brain injury. Promoting brain edema results in death. Brain contusion after ethanol injection did not cause any release in proinflammatory cytokines and activation of NF-kappaB, a cell survival signal transcription factor. N-acetyl cystine treatment after TBI reduced brain edema to keep survival.6. We established a model with steroid-induced osteonecrosis of femoral head. In this model, TLR4 signaling plays a crucial role in osteonecrosis of femoral head.