Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine, Yonago 683-8503, Japan.
J Clin Biochem Nutr. 2010 Jan;46(1):43-51. doi: 10.3164/jcbn.09-60. Epub 2009 Dec 29.
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.
波拉普利锌是一种由锌和左旋肉碱组成的螯合物,临床上用作治疗胃溃疡的药物。已有研究表明,诱导热休克蛋白(HSP)的表达参与了波拉普利锌对胃黏膜损伤的保护作用。本研究旨在探讨波拉普利锌及其成分是否能诱导 HSP70 的表达,从而预防对乙酰氨基酚(APAP)对小鼠原代培养肝细胞的毒性作用。将肝细胞用浓度为 100μM 的波拉普利锌、硫酸锌或左旋肉碱处理 9 小时,然后用 10mMAPAP 处理。结果发现,波拉普利锌或硫酸锌能增加细胞 HSP70 的表达,但左旋肉碱对此没有影响。APAP 处理前用波拉普利锌或硫酸锌预处理能显著抑制细胞死亡和细胞脂质过氧化。相反,APAP 处理后,波拉普利锌预处理并不影响细胞内谷胱甘肽的减少。此外,用 HSP 抑制剂 KNK437 处理可减弱波拉普利锌诱导的 HSP70 表达的增加,并消除波拉普利锌对 APAP 引起的细胞死亡的保护作用。这些结果表明,波拉普利锌,特别是其锌成分,能诱导小鼠原代培养肝细胞中 HSP70 的表达,并抑制 APAP 处理后的脂质过氧化,从而起到预防 APAP 毒性的作用。