Protective Effects of Lactobacillus plantarum CCFM8610 against Chronic Cadmium Toxicity in Mice Indicate Routes of Protection besides Intestinal Sequestration

Protective Effects of Lactobacillus plantarum CCFM8610 against Chronic Cadmium Toxicity in Mice Indicate Routes of Protection besides Intestinal Sequestration
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植物乳杆菌 CCFM8610 对小鼠慢性镉中毒的保护作用表明除肠隔离外的保护途径

DOI:
10.1128/aem.00762-14
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发表时间:
2014-04
影响因子:
4.4
通讯作者:
Chen Wei
Chen Wei
中科院分区:
生物学2区
文献类型:
--
作者:
Zhai Qixiao;Wang Gang;Zhao Jianxin;Liu Xiaoming;Narbad Arjan;Chen Yong Q.;Zhang Hao;Tian Fengwei;Chen Wei

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摘要我们先前的研究证实了植物乳杆菌CCFM8610对小鼠急性镉(Cd)毒性的保护作用。本研究旨在评价CCFM8610对小鼠慢性镉中毒的保护作用,并了解该菌株的保护模式。实验小鼠分成两组,分别通过饮水和腹腔注射镉染毒8周。两组均进一步分为4个亚组:对照组、单纯CD组、单纯CCFM8610组和CD+CCFM8610组。测量了粪便、肝脏和肾脏中的镉水平,并注意到了镉毒性的几个生物标志物的变化。结果表明,口服Cd后,Cd与CCFM8610共处理可有效减少Cd在肠道的吸收,减少Cd在组织中的蓄积,减轻组织氧化应激,逆转肝肾损伤,改善相应的组织病理学改变。当Cd被引入到腹膜内时,CCFM8610对组织中Cd的积累没有影响,也没有逆转抗氧化酶的活性。然而,CCFM8610仍然提供了对氧化应激的保护作用,并逆转了镉毒性生物标志物和组织病理学的变化。这些结果提示CCFM8610对小鼠慢性镉中毒有明显的拮抗作用。除了肠道镉的封存,CCFM8610治疗对镉诱导的氧化应激具有直接的保护作用。我们还提供了证据,证明后者不太可能是通过保护Cd诱导的抗氧化酶活性改变来调节的。
ABSTRACT Our previous study confirmed the ability of Lactobacillus plantarum CCFM8610 to protect against acute cadmium (Cd) toxicity in mice. This study was designed to evaluate the protective effects of CCFM8610 against chronic Cd toxicity in mice and to gain insights into the protection mode of this strain. Experimental mice were divided into two groups and exposed to Cd for 8 weeks via drinking water or intraperitoneal injection. Both groups were further divided into four subgroups, control, Cd only, CCFM8610 only, and Cd plus CCFM8610. Levels of Cd were measured in the feces, liver, and kidneys, and alterations of several biomarkers of Cd toxicity were noted. The results showed that when Cd was introduced orally, cotreatment with Cd and CCFM8610 effectively decreased intestinal Cd absorption, reduced Cd accumulation in tissue, alleviated tissue oxidative stress, reversed hepatic and renal damage, and ameliorated the corresponding histopathological changes. When Cd was introduced intraperitoneally, administration of CCFM8610 did not have an impact on tissue Cd accumulation or reverse the activities of antioxidant enzymes. However, CCFM8610 still offered protection against oxidative stress and reversed the alterations of Cd toxicity biomarkers and tissue histopathology. These results suggest that CCFM8610 is effective against chronic cadmium toxicity in mice. Besides intestinal Cd sequestration, CCFM8610 treatment offers direct protection against Cd-induced oxidative stress. We also provide evidence that the latter is unlikely to be mediated via protection against Cd-induced alteration of antioxidant enzyme activities.
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