ストスと細胞応答　　敗血症性多臓器機能障害におけるストレス応答

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  • Stress and Redox Regulation. Heat shock response in a rat model of septic multiple organ dysfunction syndrome.
  • ハイケツショウセイ タゾウキ キノウ ショウガイ ニ オケル ストレス オウトウ
  • ストレスと細胞応答

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Severe sepsis is known to result in multiple organ dysfunction syndrome (MODS), which is thought to be mediated by oxidative stress, as a result of excessive systemic inflammation. Heme Oxygenase-1 (HO-1), the rate limiting enzyme in heme catabolism, is also known as HSP32. HO-1 is induced not only by its substrate heme but also by oxidative stress. We investigated gene expression of HO-1 and physiological significance of HO-1 induction in a rat model of septic MODS induced by intraperitoneal injection of bacterial lipopolysaccharide (LPS). Following administration of LPS, HO-1 mRNA was significantly induced in the liver, lung and kidney in an organ-specific manner. Hepatic HO-1 induction appears to be mediated by an increase in hepatic free heme concentration. Inhibition of HO-1 activity by tin mesoporphyrin significantly exacerbated lung injury. These results suggest that HO-1 induction may play an important role in conferring protection on cells from oxidative damage not only by catalyzing heme, a pro-oxidant, but also by producing bilirubin, an anti-oxidant. Furthermore, HO-1 mRNA is induced markedly in the buffy coat of the blood at 3 h after LPS administration, coinciding with the increase in serum IL-6 level, suggesting that HO-1 may be one of the key markers of septic MODS.

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  • 日本薬理学雑誌

    日本薬理学雑誌 114 (5), 295-302, 1999

    公益社団法人 日本薬理学会

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