Pre-protective effect of lipoic acid on injury induced by H2O2 in IPEC-J2 cells

Cai, Xuan; Chen, Xiaolian; Wang, Xiaochun; Xu, Chunjie; Guo, Qi; Zhu, Lihui; Zhu, Siyi; Xu, Jianxiong

doi:10.1007/s11010-013-1595-9

Cited by 42 publications

(38 citation statements)

References 38 publications

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“…Cai et al, reported that 10 µg/mL LA significantly increased the cytoactivity (MTT assay) of H 2 O 2 -stressed IPEC-J2 cells [31]. This differs from our findings where we observed no effect on cell viability of LA.…”

Section: Discussioncontrasting

confidence: 99%

“…Finally, GA and LA pre-treatments were unable to significantly decrease the intracellular oxidative stress in IPEC-J2 cells. Previous research showed that LA pre-treatment had the tendency to decrease iROS in IPEC-J2 cells; however, this was not significant [31]. This study showed that GA increased the viability of H 2 O 2 stressed cells but was unable to significantly decrease iROS.…”

Section: Discussioncontrasting

confidence: 58%

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In Vitro Investigation of Six Antioxidants for Pig Diets

et al. 2016

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Oxidative stress in the small intestinal epithelium can lead to barrier malfunction. In this study, the effect of rosmarinic acid (RA), quercetin (Que), gallic acid (GA), lipoic acid (LA), ethoxyquin (ETQ) and Se-methionine (SeMet) pre-treatments using 2 mM Trolox as a control on the viability and the generation of intracellular reactive oxygen species (iROS) of oxidatively (H2O2) stressed intestinal porcine epithelial cells (IPEC-J2) was investigated. A neutral red assay showed that RA (50–400 µM), Que (12.5–200 µM), GA (50–400 µM), ETQ (6.25–100 µM), and SeMet (125–1000 µM) pre-treatments but not LA significantly increased the viability of H2O2-stressed IPEC-J2 cells (p < 0.05). A 5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate, acetyl ester (CM-H2DCFDA) fluorescent probe showed that RA (100–600 µM), Que (25–800 µM), ETQ (3.125–100 µM) and SeMet (500–2000 µM) pre-treatments significantly reduced iROS in IPEC-J2 monolayers (p < 0.05). Moreover, RA and Que were most effective in reducing iROS. Therefore, the effects of RA and Que on barrier functioning in vitro were examined. RA and Que pre-treatments significantly decreased fluorescein isothiocyanate (FITC)-conjugated dextran-4 (4 kDa) permeability and transepithelial electrical resistance (TEER) of an IPEC-J2 cell monolayer (p < 0.05). These in vitro results of RA and Que hold promise for their use as antioxidants in pig feed.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 58%

In Vitro Investigation of Six Antioxidants for Pig Diets

et al. 2016

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“…Fe 2+ binding may attenuate oxidative stress and inhibit Fe 2+ -induced lipid peroxidation from iron overload. On the other hand, H 2 O 2 can significantly increase the intracellular free radicals, leading to serious DNA damage and significantly reduce superoxide dismutase, glutathione peroxidase, catalase, and lipase activity [27]. So ferrous iron chelatorclioquinol-may prevent its happening and reduce brain edema, but it would not happen with ferric iron chelatordeferiprone.…”

Section: Discussionmentioning

confidence: 99%

Effect Comparison of Both Iron Chelators on Outcomes, Iron Deposit, and Iron Transporters After Intracerebral Hemorrhage in Rats

Wang

Tang

et al. 2015

Mol Neurobiol

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Iron overload plays a key role in brain injury after intracerebral hemorrhage (ICH). We explored the roles of ferric iron chelator-deferiprone (DFP)-and ferrous iron chelator-clioquinol (CQ)-in ICH rats through the outcomes, iron deposits, reactive oxygen species (ROS), brain water content, and related iron transporters. One hundred eight Sprague-Dawley rats received intra-striatal infusions of 0.5 U of type IV collagenase to establish ICH models. The rats were randomly assigned to the sham, vehicle, DFP, and CQ groups. We evaluated the outcomes, iron levels, brain water content, and ROS; meanwhile, immunohistochemistry and real-time quantitative polymerase chain reaction (RT-qPCR) were utilized to determine ferritin, transferrin, transferrin receptor, divalent metal transport 1 (DMT1), and ferroportin at 48 and 72 h, 7 and 14 days after surgery. Our results showed ICH induced iron overload, brain edema, ROS formation, and neurological deficits. Both iron chelators decreased iron levels; CQ improved the neurological outcome, attenuated brain edema, and ROS production. DFP reduced iron contents but not brain water content and ROS generation. DFP failed to improve the outcome. ICH initiated endogenous iron chelators and transporters, both exogenous iron chelators enhanced expression of transferrin and transferrin receptor. CQ enhanced expression of ferroportin but not DMT1, while DFP enhanced expression of DMT1 but not ferroportin. Ferrous iron contributed to brain injury, and binding ferrous iron can modestly improve outcome after ICH in rats. The exogenous ferrous iron chelator possibly functioned via endogenous ferrous iron transporters on ICH. Therefore, ferrous iron may be a promising target for ICH in future.

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“…The incidence of inflammatory bowel disease is closely related to the oxidative stress generated by intestinal epithelia. The incidence of oxidative stress can cause intestinal epithelial cell damage; ROS can induce the activation of a variety of signaling pathways to promote intestinal epithelial cell apoptosis, including the PI3K pathway, which plays an important role in this process (84,85). The Jak/STAT3 and PI3K/Akt pathways are closely associated with the IL-6 receptor family; thus, it can be hypothesized that apelin/oxidative stress promotes the occurrence and development of intestinal inflammation, and may be related to the IL-6 receptor family.…”

Section: Apelin Regulates Oxidative Stress In the Occurrence Of Othermentioning

confidence: 99%

Apelin/APJ system: A novel therapeutic target for oxidative stress-related inflammatory diseases (Review)

Zhou

Cao

Chen

2016

International Journal of Molecular Medicine

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Abstract. Apelin, the endogenous ligand of APJ which is a member of G protein-coupled receptors, has been shown to be expressed in a variety of tissues in vivo and to exert significant biological effects. Studies have indicated that the apelin/APJ system is involved in the regulation of a variety of physiological functions and pathological processes, and that it is associated with cardiovascular diseases (such as atherosclerosis, hypertension, heart failure and myocardial injury), diabetes with microvascular complications, ischemia reperfusion injury, tumors, pre-eclampsia, as well as others. The occurrence of these diseases is closely related to endothelial dysfunction and the local inflammatory response; however, the occurrence of oxidative stress is related to vascular injury, due to the excessive generation of reactive oxygen species (ROS) and can lead to vascular damage and a series of inflammatory reactions. Therefore, this review summarizes the association between apelin/APJ, oxidative stress and inflammation-related diseases. In addition, drugs targeting the apelin/APJ system are recommended, thus providing a novel therapeutic strategy for oxidative stress-related inflammatory diseases.

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Pre-protective effect of lipoic acid on injury induced by H2O2 in IPEC-J2 cells

Cited by 42 publications

References 38 publications

In Vitro Investigation of Six Antioxidants for Pig Diets

In Vitro Investigation of Six Antioxidants for Pig Diets

Effect Comparison of Both Iron Chelators on Outcomes, Iron Deposit, and Iron Transporters After Intracerebral Hemorrhage in Rats

Apelin/APJ system: A novel therapeutic target for oxidative stress-related inflammatory diseases (Review)

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