Protective effects of baicalin on LPS-induced injury in intestinal epithelial cells and intercellular tight junctions

Chen, Jian; Zhang, Ren; Wang, Jian; Yu, Peng; Liu, Quan; Zhang, Dan; Hou-pan, Song; Kuang, Zaoyuan

doi:10.1139/cjpp-2014-0262

Cited by 45 publications

(35 citation statements)

References 26 publications

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“…ZO-1 was the first TJ protein to be discovered (45) and is directly associated with occludin, serving an important role in regulating TJ barrier function (46). It has been reported that LPS is able to decrease the expression of ZO-1 and occludin (47), which is consistent with the results of the present study.…”

Section: Discussionsupporting

confidence: 94%

Bletilla�striata polysaccharide has a protective effect on intestinal epithelial barrier disruption in TAA‑induced cirrhotic rats

et al. 2018

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It has been reported that intestinal epithelial barrier dysfunction serves an important role in the development of liver cirrhosis. However, at present there is no satisfactory treatment for intestinal mucosal lesions and ulcers associated with cirrhosis. The aim of the present study was to investigate the effect of Bletilla striata polysaccharide (BSP) on intestinal epithelial barrier disruption in rats with thioacetamide (TAA)-induced liver cirrhosis. Rats were randomly divided into 5 groups (n=10): BSP low dosage (15 mg/kg), BSP middle dosage (30 mg/kg), BSP high dosage (60 mg/kg), experiment and control groups. All groups except control group were administered with TAA (200 mg/kg/day) to induce liver cirrhosis. Following modeling, rats in the low, middle and high-dose BSP groups received BSP. ELISA kits were used to measure the endotoxin, alanine transaminase (ALT) and aspartate transaminase (AST) levels in the portal vein, while interleukin (IL)-6 and tumor necrosis factor (TNF)-α expression in the ileal tissue was measured. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to detect the expression of zonula occludens (ZO)-1 and occludin mRNA and protein, respectively. Intestinal epithelial tissue pathology was detected using hematoxylin-eosin (HE) staining. Immunohistochemistry was performed to assess the expression of ZO-1 and occludin in intestinal epithelial tissues. Following treatment with BSP, ALT, AST and endotoxin levels in the portal vein, as well as IL-6 and TNF-α expression in ileal tissues, were significantly decreased compared with model group (P<0.05 or 0.01). Furthermore, BSP treatment upregulated the expression of ZO-1 and occludin mRNA and protein compared with the model group (P<0.05 or 0.01) and cytoplasmic staining for these proteins was increased. The degree of intestinal epithelial tissue pathological damage was significantly reduced in the BSP groups. In conclusion, BSP is able to reduce endotoxin levels, inhibit the inflammatory cytokines IL-6 and TNF-α and elevate expression of ZO-1 and occludin at tight junctions. Together, these results suggest a novel protective agent for the restoration of intestinal epithelial barrier disruption.

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Section: Discussionsupporting

confidence: 94%

Bletilla�striata polysaccharide has a protective effect on intestinal epithelial barrier disruption in TAA‑induced cirrhotic rats

et al. 2018

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“…The failure of intestinal barrier function induced with LPS resulted in an increase in mucosal permeability, which was hypothesized to be a major promoter of bacterial translocation and inflammatory cytokines release[30,31]. IL-6 and TNF-α are the critical cytokines involved in inflammation, and bifidobacterium is regarded as a common treatment strategy for information-related diseases, including NEC [22,32,33].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Bifidobacterium on Intestinal Barrier Function in LPS-Induced Enterocyte Barrier Injury of Caco-2 Monolayers and in a Rat NEC Model

et al. 2016

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Zonulin protein is a newly discovered modulator which modulates the permeability of the intestinal epithelial barrier by disassembling intercellular tight junctions (TJ). Disruption of TJ is associated with neonatal necrotizing enterocolitis (NEC). It has been shown bifidobacterium could protect the intestinal barrier function and prophylactical administration of bifidobacterium has beneficial effects in NEC patients and animals. However, it is still unknown whether the zonulin is involved in the gut barrier dysfunction of NEC, and the protective mechanisms of bifidobacterium on intestinal barrier function are also not well understood. The present study aims to investigate the effects of bifidobacterium on intestinal barrier function, zonulin regulation, and TJ integrity both in LPS-induced enterocyte barrier injury of Caco-2 monolayers and in a rat NEC model. Our results showed bifidobacterium markedly attenuated the decrease in transepithelial electrical resistance and the increase in paracellular permeability in the Caco-2 monolayers treated with LPS (P < 0.01). Compared with the LPS group, bifidobacterium significantly decreased the production of IL-6 and TNF-α (P < 0.01) and suppressed zonulin release (P < 0.05). In addition, bifidobacterium pretreatment up-regulated occludin, claudin-3 and ZO-1 expression (P < 0.01) and also preserved these proteins localization at TJ compared with the LPS group. In the in vivo study, bifidobacterium decreased the incidence of NEC from 88 to 47% (P < 0.05) and reduced the severity in the NEC model. Increased levels of IL-6 and TNF-α in the ileum of NEC rats were normalized in bifidobacterium treated rats (P < 0.05). Moreover, administration of bifidobacterium attenuated the increase in intestinal permeability (P < 0.01), decreased the levels of serum zonulin (P < 0.05), normalized the expression and localization of TJ proteins in the ileum compared with animals with NEC. We concluded that bifidobacterium may protect against intestinal barrier dysfunction both in vitro and in NEC. This protective effect is associated with inhibition of proinflammatory cytokine secretion, suppression of zonulin protein release and improvement of intestinal TJ integrity.

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“…16) Orally administered baicalin inhibits the expression of TNF-α in mice injected with LPS via regulating the activation of the transcription factor nuclear factor-kappaB (NF-κB). 39) Moreover, high levels of TNF-α following LPS stimulation were associated with severe loss of ZO-1 in the ileum.…”

Section: Discussionmentioning

confidence: 99%

“…16) Briefly, cells were grown in complete Dulbecco's modified Eagle's medium (DMEM; Hyclone) at 37°C in 5% CO 2 and were then subcultured after digestion with 0.25% trypsin in phosphate buffered saline (PBS).…”

Section: Methodsmentioning

confidence: 99%

“…[13][14][15] We have shown earlier that baicalin reversed the down-regulation of the TJ protein ZO-1 and decreased TNF-α level after lipopolysaccharide (LPS) stimulation injury of IEC-6 (rat small intestinal epithelial cells), thereby maintaining the integrity of endothelial barriers. 16) However, whether baicalin has direct protective effect against TNF-α-induced injury in intestinal TJs is not known and the mechanisms that mediate the effects of baicalin on ZO- 1 have not yet been investigated.…”

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confidence: 99%

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Baicalin Protects against TNF-α-Induced Injury by Down-Regulating miR-191a That Targets the Tight Junction Protein ZO-1 in IEC-6 Cells

Wang

Ren

Chen

et al. 2017

Biological & Pharmaceutical Bulletin

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Protective effects of baicalin on LPS-induced injury in intestinal epithelial cells and intercellular tight junctions

Abstract: Baicalin has the capacity to protect IEC-6 cells and the intercellular tight junctions from LPS-induced injury. The mechanisms may be associated with inhibiting the production of inflammatory cytokines, and up-regulating the mRNA and protein expression of ZO-1.

Cited by 45 publications

References 26 publications

Bletilla�striata polysaccharide has a protective effect on intestinal epithelial barrier disruption in TAA‑induced cirrhotic rats

Bletilla�striata polysaccharide has a protective effect on intestinal epithelial barrier disruption in TAA‑induced cirrhotic rats

Protective Effects of Bifidobacterium on Intestinal Barrier Function in LPS-Induced Enterocyte Barrier Injury of Caco-2 Monolayers and in a Rat NEC Model

Baicalin Protects against TNF-α-Induced Injury by Down-Regulating miR-191a That Targets the Tight Junction Protein ZO-1 in IEC-6 Cells

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