Characterization of <i>in vitro</i> effects of microcystin‐LR on intestinal epithelial cells

Zhou, Yuan; Xu, Xiaoping; Yu, Beibei; Yu, Guang

doi:10.1002/tox.22375

Cited by 23 publications

(14 citation statements)

References 39 publications

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“…After exposure of 0-50 μmol/L of MC-LR concentrations for 24 h in IEC-6 cells, the intracellular localization of MC-LR was in the cytoplasm and around the nucleus. Furthermore, western blot results revealed that there was a dose-dependent content following exposure to MC-LR[ 18 ].…”

Section: Concentration or Localization Of Mcs In The Small Intestinementioning

confidence: 99%

“…Previous studies indicated that MCs can be transported across enterocyte membranes via OATPs[ 2 ]. Moreover, studies have manifested that cell viability significantly decreased, while the ratio of apoptotic cells increased, after intestinal epithelial cells (IEC-6) and human intestinal Caco-2 cells were exposed to MCs[ 18 ]. MCs can affect the integrity of the intestinal barrier by decreasing its transepithelial electrical resistance (TEER) values and inducing the cytoskeletal protein expression of occludin and ZO-1 in IECs in a dose-dependent decrease[ 18 ].…”

Section: Pathological Effect Of Mcs In the Intestinesmentioning

confidence: 99%

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Gastrointestinal toxicity induced by microcystins

Huang

Yang

et al. 2018

WJCC

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Microcystins (MCs) are produced by certain bloom-forming cyanobacteria that can induce toxicity in various organs, including renal toxicity, reproductive toxicity, cardiotoxicity, and immunosuppressive effects. It has been a significant global environmental issue due to its harm to the aquatic environment and human health. Numerous investigators have demonstrated that MC exposure can induce a widespread epidemic of enterogastritis with symptoms similar to food poisoning in areas close to lakes. Both in vivo and in vitro studies have provided evidence of positive associations between MC exposure and gastrointestinal toxicity. The toxicity of MCs on the gastrointestinal tract is multidimensional. MCs can affect gastrointestinal barrier function and shift the structure of gut microbiota in different gut regions. Furthermore, MCs can inhibit the secretion of gastrointestinal digestive enzymes and the release of inflammatory cytokines, which affects the expression of immune-related genes in the intestine. The damage of the intestine is closely correlated to MC exposure because the intestine is the main site for the digestion and absorption of nutrients. The damage to the gastrointestinal tract due to MCs was summarized from different aspects, which can be used as a foundation for further exploration of molecular damage mechanisms.

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Section: Concentration or Localization Of Mcs In The Small Intestinementioning

confidence: 99%

Section: Pathological Effect Of Mcs In the Intestinesmentioning

confidence: 99%

Gastrointestinal toxicity induced by microcystins

Huang

Yang

et al. 2018

WJCC

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“…3 Recent studies demonstrate that MC-LR has toxic effect on the intestine. 4 However, the mechanism of this phenomenon is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Effects of Chronic Exposure to Microcystin-LR on the Gut Microbiota of Male Mice

Zhuang

Jin

et al. 2020

Int J Toxicol

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Increasing evidence indicates that environmental pollutants can change human gut microbiota. Microcystin–leucine arginine (MC-LR), considered a major hazard to mammals, is one of the important contaminants. However, little is known about the long-term influence of MC-LR on gut microbial communities. We aimed to investigate the effect of MC-LR on gut microbiota composition and functions by conducting a chronic exposure of male mice to MC-LR via the oral route. Using 16S rRNA gene sequencing analysis on cecum samples of mice, our results showed that significant changes of species diversity were observed in the gut microbiota of MC-LR-exposed mice. In addition, comparative analysis of the microbial communities showed that the reduction of the Actinobacteria and Saccharibacteria populations was detected in MC-LR-exposed mice. Collectively, our study highlighted the significant effects of MC-LR on the shift of gut microbial communities which could contribute to the development of metabolic syndromes.

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“…These cells have microvilli, centrioles, Golgi complexes, and junctional complexes according to an ultrastructural study ( Quaroni et al, 1979 ). Due to the characteristics of IEC-6 cells, this cell line has also been used in studies of hepatotoxicity ( Zhou et al, 2017 ), tight junctions ( Yu et al, 2016 ) and TRP channels ( Kono et al, 2013 ; Yamawaki et al, 2014 ). Cells were transiently transfected with plasmid to produce TRPV1- overexpressing and TRPV1-knockdown cells.…”

Section: Discussionmentioning

confidence: 99%

Novobiocin, a Newly Found TRPV1 Inhibitor, Attenuates the Expression of TRPV1 in Rat Intestine and Intestinal Epithelial Cell Line IEC-6

Liang

Cai

et al. 2018

Front. Pharmacol.

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Background and Purpose: Novobiocin (NOVO), an ABC transporter inhibitor, decreases intestinal wall permeability of capsaicin (CAP), an ABC transporter substrate. However, the mechanism of this effect is not consistent with the action of NOVO as an ABC transporter inhibitor. We previously found that CAP can also be transported via TRPV1, which was site-specific in the permeability of CAP across the intestine. We explored the regulation by NOVO of TRPV1 in the present study.Methods: Rats and transfected IEC-6 cells were used as the models to assess intestinal permeability and expression of TRPV1. Ussing chamber and intracellular accumulation were used to evaluate the influence of NOVO on the transport of CAP in vitro. The expression of TRPV1 was detected after administration of NOVO by qRT-PCR, western blot and immunofluorescent imaging. In addition, MTT and lactate dehydrogenase (LDH) were used to evaluate the cytotoxicity of NOVO in both rat and cell models. Finally, the effect of NOVO on the absorption of CAP in vivo was studied by LC-MS/MS.Results: In vitro data showed that there existed a dose-dependent relationship in the range of concentration between 5 and 50 μM, and even 5 μM NOVO could decrease intestinal permeability of CAP across the intestine. Meanwhile, cytosolic accumulation of CAP decreased when NOVO was used simultaneously or 24 h in advance. NOVO exhibited an inhibition level similar to that of ruthenium red (RR) or SB-705498, a TRPV1-specific inhibitor. NOVO down-regulated TRPV1 expression in the intestine and in transfected cells in a concentration-dependent fashion, hinting that its inhibition of the permeability of CAP is due to its inhibition of TRPV1 expression. Immunofluorescent imaging data showed that the fluorescence intensity of TRPV1 was reduced after pre-treatment with NOVO and SB-705498. In vivo data further demonstrated that oral co-administration of NOVO decreased Cmax and AUC of CAP in dosage-dependent ways, consistent with its role as a TRPV1 inhibitor.Conclusion: NOVO could be a potential TRPV1 inhibitor by attenuating the expression of TRPV1 and may be used to attenuate permeability of TRPV1 substrates.

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Characterization of in vitro effects of microcystin‐LR on intestinal epithelial cells

Cited by 23 publications

References 39 publications

Gastrointestinal toxicity induced by microcystins

Gastrointestinal toxicity induced by microcystins

Effects of Chronic Exposure to Microcystin-LR on the Gut Microbiota of Male Mice

Novobiocin, a Newly Found TRPV1 Inhibitor, Attenuates the Expression of TRPV1 in Rat Intestine and Intestinal Epithelial Cell Line IEC-6

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