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Intervention of Grape Seed Proanthocyanidin Extract on the Subchronic Immune Injury in Mice Induced by Aflatoxin B1

机译:葡萄籽原花青素提取物对黄曲霉毒素B1致小鼠亚慢性免疫损伤的干预作用

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摘要

The aim was to investigate the prevention of grape seed proanthocyanidin extract (GSPE) on the subchronic immune injury induced by aflatoxin B1 (AFB1) and the possible ameliorating effect of GSPE in mice. The subchronic AFB1-induced immune injury mice model was set up with the continuous administration of 100 μg/kg body weight (BW) AFB1 for six weeks by intragastric administration. Then, intervention with different doses (50 and 100 mg/kg BW) of GSPE was conducted on mice to analyze the changes of body weight, immune organ index, antioxidant capability of spleen, serum immunoglobulin content, and the expression levels of inflammatory cytokines. The prevention of GSPE on the immune injury induced by AFB1 was studied. The GSPE could relieve the AFB1-induced reduction of body weight gain and the atrophy of the immune organ. The malondialdehyde (MDA) level of the spleen in the AFB1 model group significantly increased, but levels of catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-PX), and superoxide dismutase (SOD) significantly decreased. The GSPE could significantly inhibit the oxidative stress injury of the spleen induced by AFB1. AFB1 exposure could not significantly change the contents of IgA, IgG, or IgM. AFB1 significantly improved the expression of interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ). Additionally, GSPE could decrease the expression of these four proinflammatory factors to different degrees and inhibit the inflammatory reaction of mice. The results suggest that GSPE alleviates AFB1-induced oxidative stress and significantly improves the immune injury of mice induced by AFB1.
机译:目的是研究葡萄籽原花青素提取物(GSPE)对黄曲霉毒素B1(AFB1)引起的亚慢性免疫损伤的预防作用以及GSPE对小鼠的改善作用。建立亚慢性AFB1诱导的免疫损伤小鼠模型,并通过胃内给药连续六周施用100μg/ kg体重(BW)AFB1。然后,以不同剂量(50和100 mg / kg体重)的GSPE对小鼠进行干预,以分析体重,免疫器官指数,脾脏抗氧化能力,血清免疫球蛋白含量以及炎性细胞因子表达水平的变化。研究了GSPE对AFB1诱导的免疫损伤的预防作用。 GSPE可以缓解AFB1引起的体重增加减少和免疫器官萎缩。 AFB1模型组的脾脏丙二醛(MDA)水平显着升高,但过氧化氢酶(CAT),谷胱甘肽(GSH),谷胱甘肽过氧化物酶(GSH-PX)和超氧化物歧化酶(SOD)的水平显着降低。 GSPE可以显着抑制AFB1引起的脾脏氧化应激损伤。 AFB1暴露不会显着改变IgA,IgG或IgM的含量。 AFB1显着改善白介素1β(IL-1β),IL-6,肿瘤坏死因子α(TNF-α)和干扰素γ(IFN-γ)的表达。另外,GSPE可以不同程度降低这四种促炎因子的表达并抑制小鼠的炎症反应。结果表明,GSPE可减轻AFB1诱导的氧化应激,并显着改善AFB1诱导的小鼠免疫损伤。

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