Polaprezinc Protects Mice against Endotoxin Shock

DOI PubMed 4 Citations 45 References Open Access
  • Ohata Shuzo
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine
  • Moriyama Chihiro
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine
  • Yamashita Atsushi
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine
  • Nishida Tadashi
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine
  • Kusumoto Chiaki
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine
  • Mochida Shinsuke
    Division of Anesthesiology and Critical Care Medicine, Department of Surgery, Tottori University Faculty of Medicine
  • Minami Yukari
    Division of Anesthesiology and Critical Care Medicine, Department of Surgery, Tottori University Faculty of Medicine
  • Nakada Junya
    Department of Anesthesiology, Aichi Cancer Center Hospital
  • Shomori Kohei
    Division of Organ Pathology, Department of Microbiology and Pathology, Tottori University Faculty of Medicine
  • Inagaki Yoshimi
    Division of Anesthesiology and Critical Care Medicine, Department of Surgery, Tottori University Faculty of Medicine
  • Ohta Yoshiji
    Department of Chemistry, School of Medicine, Fujita Health University
  • Matsura Tatsuya
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine

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Polaprezinc (PZ), a chelate compound consisting of zinc and <sc>l</sc>-carnosine (Car), is an anti-ulcer drug developed in Japan. In the present study, we investigated whether PZ suppresses mortality, pulmonary inflammation, and plasma nitric oxide (NO) and tumor necrosis factor (TNF)-α levels in endotoxin shock mice after peritoneal injection of lipopolysaccharide (LPS), and how PZ protects against LPS-induced endotoxin shock. PZ pretreatment inhibited the decrease in the survival rate of mice after LPS injection. PZ inhibited the increases in plasma NO as well as TNF-α after LPS. Compatibly, PZ suppressed LPS-induced inducible NO synthase mRNA transcription in the mouse lungs. PZ also improved LPS-induced lung injury. However, PZ did not enhance the induction of heat shock protein (HSP) 70 in the mouse lungs after LPS. Pretreatment of RAW264 cells with PZ suppressed the production of NO and TNF-α after LPS addition. This inhibition likely resulted from the inhibitory effect of PZ on LPS-mediated nuclear factor-κB (NF-κB) activation. Zinc sulfate, but not Car, suppressed NO production after LPS. These results indicate that PZ, in particular its zinc subcomponent, inhibits LPS-induced endotoxin shock via the inhibition of NF-κB activation and subsequent induction of proinflammatory products such as NO and TNF-α, but not HSP induction.<br>

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