Grape seed proanthocyanidins protects against cadmium induced oxidative pancreatitis in rats by attenuating oxidative stress, inflammation and apoptosis via Nrf-2/HO-1 signaling
Grape seed proanthocyanidins protects against cadmium induced oxidative pancreatitis in rats by attenuating oxidative stress, inflammation and apoptosis via Nrf-2/HO-1 signaling
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DOI：
10.1016/j.jnutbio.2016.03.001
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发表时间：
2016-06-01
影响因子：
5.6
通讯作者：
Miltonprabu, Selvaraj
中科院分区：
文献类型：
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作者：
Bashir, Nazima;Manoharan, Vaihundam;Miltonprabu, Selvaraj
本研究旨在探讨葡萄籽原花青素(GSP)在镉(Cd)诱导的大鼠胰腺细胞氧化应激毒性中的作用。4组健康大鼠口服镉(5 mg/kgbw)，为探讨GSP100 mg/kgbw的作用机制，在镉中毒前90min给予GSP100 mg/kg。采用多种生化分析、组织学、Western blotting和ELISA法对CD的发病机制进行分子和细胞机制的研究。镉中毒大鼠胰腺促炎细胞因子(TNF-α、IL-1β和干扰素-γ)水平升高，细胞防御蛋白(NRF-2和HO-1)和葡萄糖转运蛋白(GLUT-2和GLUT-4)水平降低，细胞凋亡信号分子Caspase-12/9/8/3水平升高。结果提示，GSP治疗可降低血糖水平，升高血浆胰岛素水平，减轻氧化应激相关指标。GSP通过减轻炎症反应和抑制细胞凋亡来保护胰腺组织。GSP的这种独特性和没有任何可检测到的不良反应表明，它有可能作为一种有效的保护剂，用于治疗氧化应激介导的大鼠胰腺功能障碍。(C)2016 Elsevier Inc.保留所有权利。
The present study has been designed and carried out to explore the role of grape seed proanthocyanidins (GSP) in the pancreas of cadmium (Cd)-induced cellular oxidative stress-mediated toxicity in rats. Four groups of healthy rats were given oral doses of Cd (5-mg/kg BW) and to identify the possible mechanism of action of GSP 100-mg/kg BW was selected and was given 90 min before Cd intoxication. The causative molecular and cellular mechanism of Cd was determined using various biochemical assays, histology, western blotting and ELISA. Cd intoxication revealed increased levels of proinflammatory cytokines (TNF-alpha, IL1 beta and IFN-gamma), reduced levels of cellular defense proteins (Nrf-2 and HO-1) and glucose transporter (GLUT-2 and GLUT-4) along with the enhanced levels of signaling molecules of apoptosis (cleaved Caspase-12/9/8/3) in the pancreas of Cd-intoxicated rats. Results suggested that the treatment with GSP reduced blood glucose level, increased plasma insulin and mitigated oxidative stress-related markers. GSP protects pancreatic tissue by attenuated inflammatory responses and inhibited apoptosis. This uniqueness and absence of any detectable adverse effect of GSP proposes the possibility of using it as an effective protector in the oxidative stress-mediated pancreatic dysfunction in rats. (C) 2016 Elsevier Inc. All rights reserved.