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羟基柠檬酸改善雄性Wistar大鼠中高果糖诱导的氧化还原失衡和应激敏感激酶的激活。

Hydroxycitric acid ameliorates high-fructose-induced redox imbalance and activation of stress sensitive kinases in male Wistar rats.

作者信息

Sripradha Ramalingam, Sridhar Magadi Gopalakrishna, Maithilikarpagaselvi Nachimuthu

出版信息

J Basic Clin Physiol Pharmacol. 2016 Jun 1;27(4):349-56. doi: 10.1515/jbcpp-2014-0132.

Abstract

BACKGROUND

Excess fructose consumption causes dyslipidemia, oxidative stress, and various complications. Hydroxycitric acid (HCA), one of the principal components of the fruit Garcinia cambogia, has been shown to possess antiobesity properties. The objective was to investigate the effects of HCA on redox imbalance and activation of stress sensitive kinases in high fructose-fed rats.

METHODS

Male Wistar rats (n=40) were randomly divided into four groups with 10 rats in each group. The rats were fed with either standard rodent diet or 60% fructose diet and administered with HCA at a dose of 400 mg/kg body wt/day for 10 weeks. Body weight was measured once a week, and food intake was noted daily. At the end of the study, lipid profile and oxidative stress parameters were estimated. Expressions of stress sensitive kinases were analyzed in liver homogenates.

RESULTS

Fructose-fed rats displayed elevated body weight, higher levels of plasma total cholesterol (TC), triacylglycerol (TAG), non-high-density lipoprotein cholesterol (non HDL-C), malondialdehyde (MDA), total oxidant status (TOS), oxidative stress index (OSI), lower levels of HDL-C, glutathione (GSH), glutathione peroxidase (GPx), and total antioxidant status (TAS). Fructose feeding caused higher phosphorylation of stress sensitive kinases ERK ½ and p38. Administration with HCA lowered body weight, food intake, TAG, non-HDL-C, MDA, TOS, and OSI and elevated GSH, GPx, and TAS levels. Reduced phosphorylation of ERK ½ and p38 mitogen-activated protein kinase (MAPK) was observed upon HCA treatment.

CONCLUSIONS

Thus, HCA improved fructose induced redox imbalance and activation of stress sensitive kinases through its hypolipidemic effects.

摘要

背景

过量摄入果糖会导致血脂异常、氧化应激及各种并发症。羟基柠檬酸(HCA)是藤黄果的主要成分之一,已被证明具有抗肥胖特性。目的是研究HCA对高果糖喂养大鼠氧化还原失衡及应激敏感激酶激活的影响。

方法

将40只雄性Wistar大鼠随机分为四组,每组10只。大鼠分别喂食标准啮齿动物饲料或60%果糖饲料,并以400mg/kg体重/天的剂量给予HCA,持续10周。每周测量一次体重,每天记录食物摄入量。研究结束时,评估血脂谱和氧化应激参数。分析肝匀浆中应激敏感激酶的表达。

结果

果糖喂养的大鼠体重增加,血浆总胆固醇(TC)、三酰甘油(TAG)、非高密度脂蛋白胆固醇(非HDL-C)、丙二醛(MDA)、总氧化剂状态(TOS)、氧化应激指数(OSI)水平升高,高密度脂蛋白胆固醇(HDL-C)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GPx)和总抗氧化状态(TAS)水平降低。果糖喂养导致应激敏感激酶ERK ½和p38的磷酸化增加。给予HCA可降低体重、食物摄入量、TAG、非HDL-C、MDA、TOS和OSI,并提高GSH、GPx和TAS水平。HCA处理后观察到ERK ½和p38丝裂原活化蛋白激酶(MAPK)的磷酸化减少。

结论

因此,HCA通过其降血脂作用改善了果糖诱导的氧化还原失衡及应激敏感激酶的激活。

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