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膳食烟酸补充可改善肝脏锌摄取,并提供肝脏抗氧化损伤保护。

Dietary nicotinic acid supplementation improves hepatic zinc uptake and offers hepatoprotection against oxidative damage.

机构信息

Agharkar Research Institute, G. G. Agarkar Road, Pune 411 004, India.

出版信息

Br J Nutr. 2011 Jun 28;105(12):1741-9. doi: 10.1017/S0007114510005520. Epub 2011 Jan 25.

Abstract

We examined the effect of dietary nicotinic acid (NA) variations before and after oxidative stress (OS) treatment on the antioxidant defence system, function and morphology of the liver along with Zn status in rats. OS was generated by three intraperitoneal injections of tert-butyl hydroperoxide in the first week for the pre-exposure group and in the third week for the post-exposure group, respectively. These groups were further divided into subgroups and fed on a diet with marginally deficient Zn (10 mg Zn/kg diet) and NA variations as NA deficient, normal and excess with 10, 30 and 1000 mg NA/kg diet, respectively. Aspartate aminotransferase and alanine aminotransferase levels were elevated in rats with OS coupled with the Zn- and NA-deficient diet, which decreased towards normal with excess dietary NA. Excess NA supplementation in the OS pre-exposure group resulted in nearly preserved hepatic architecture with normal hepatocytes, whereas maximum tissue destruction was evident in the post-exposure group with NA deficiency. Dose-dependent improvement in the antioxidant defence system, enhanced reduced glutathione levels, lowered lipid peroxidation and higher hepatic Zn levels were observed with NA supplementation. The effect was more prominent in the pre-exposure group. In conclusion, dietary NA supplementation improves hepatic Zn uptake and results in hepatoprotection against OS-induced damage in rats.

摘要

我们研究了氧化应激(OS)处理前后饮食烟酸(NA)变化对大鼠抗氧化防御系统、肝脏功能和形态以及 Zn 状态的影响。OS 通过在前一周内给三组大鼠腹膜内注射叔丁基过氧化物,分别在预暴露组和后暴露组中产生。这些组进一步分为亚组,并分别用 Zn 含量略不足(10mg Zn/kg 饮食)和 NA 变化的饮食喂养,NA 缺乏、正常和过量分别为 10、30 和 1000mg/kg 饮食。与 Zn 和 NA 缺乏饮食相关,OS 大鼠的天门冬氨酸氨基转移酶和丙氨酸氨基转移酶水平升高,过量的 NA 饮食使这些酶的水平恢复正常。在 OS 预暴露组中,过量的 NA 补充几乎保留了正常肝细胞的肝组织结构,而在暴露组中,NA 缺乏时则明显发生了组织破坏。随着 NA 补充,抗氧化防御系统、还原型谷胱甘肽水平、脂质过氧化水平和肝 Zn 水平呈剂量依赖性改善。这种作用在预暴露组更为明显。总之,饮食 NA 补充可改善肝脏对 Zn 的摄取,并可防止 OS 诱导的大鼠肝损伤。

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