Zinc Supplementation with Polaprezinc Protects Mouse Hepatocytes against Acetaminophen-Induced Toxicity via Induction of Heat Shock Protein 70
| Autor: | Shinsuke Mochida, Yoshimi Inagaki, Chiaki Kusumoto, Tatsuya Matsura, Junya Nakada, Yoshiji Ohta, Tadashi Nishida, Shuzo Ohata |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Programmed cell death
hepatotoxicity Nutrition and Dietetics Clinical Biochemistry digestive oral and skin physiology zinc heat shock protein Medicine (miscellaneous) Carnosine Polaprezinc Biology Pharmacology Acetaminophen Hsp70 Lipid peroxidation chemistry.chemical_compound polaprezinc chemistry Biochemistry Heat shock protein Toxicity medicine Original Article medicine.drug acetaminophen |
| Zdroj: | Journal of Clinical Biochemistry and Nutrition |
| ISSN: | 1880-5086 0912-0009 |
| Popis: | Polaprezinc, a chelate compound consisting of zinc and l-carnosine, is clinically used as a medicine for gastric ulcers. It has been shown that induction of heat shock protein (HSP) is involved in protective effects of polaprezinc against gastric mucosal injury. In the present study, we investigated whether polaprezinc and its components could induce HSP70 and prevent acetaminophen (APAP) toxicity in mouse primary cultured hepatocytes. Hepatocytes were treated with polaprezinc, zinc sulfate or l-carnosine at the concentration of 100 microM for 9 h, and then exposed to 10 mM APAP. Polaprezinc or zinc sulfate increased cellular HSP70 expression. However, l-carnosine had no influence on it. Pretreatment of the cells with polaprezinc or zinc sulfate significantly suppressed cell death as well as cellular lipid peroxidation after APAP treatment. In contrast, pretreatment with polaprezinc did not affect decrease in intracellular glutathione after APAP. Furthermore, treatment with KNK437, an HSP inhibitor, attenuated increase in HSP70 expression induced by polaprezinc, and abolished protective effect of polaprezinc on cell death after APAP. These results suggested that polaprezinc, in particular its zinc component, induces HSP70 expression in mouse primary cultured hepatocytes, and inhibits lipid peroxidation after APAP treatment, resulting in protection against APAP toxicity. |
| Databáze: | OpenAIRE |
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