Increased expression of tight junction proteinï¿½occludin is associated with the protective effect of mosapride against aspirin‑induced gastric injury

Liu, Chenchen; Duan, Zhaotao; Guan, Yanjun; Wu, Hao; Hu, Kewei; Gao, Xin; Yuan, Fenghong; Jiang, Ziyan; Yuan, Fan; He, Bangshun; Wang, Shukui; Zhang, Zhenyu

doi:10.3892/etm.2017.5550

Cited by 7 publications

(7 citation statements)

References 26 publications

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“…It has also been reported that OCLN and ZO1 are not only capable of controlling paracellular macromolecule permeability but also interacting with intracellular signaling pathways that regulate and maintain intestinal epithelial permeability, subsequently enhancing intestinal epithelial barrier function [25][26][27][28][29]. To further understand the interaction between miR-144, OCLN/ZO1 and L. casei LC01 on regulating intestinal permeability in IECs, we transfected IECs with miR-144 and pcDNA3.1-OCLN/ZO1 under L. casei LC01 treatment.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus casei LC01 Regulates Intestinal Epithelial Permeability through miR-144 Targeting of OCLN and ZO1

Hou

Huang

Wang

et al. 2020

J. Microbiol. Biotechnol.

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Our previous report determined that miR-144 is a key regulator of intestinal epithelial permeability in irritable bowel syndrome with diarrhea (IBS-D) rats. Recent evidence has shown that lactobacilli play an important role in the relief of IBS-D symptoms. However, few studies have addressed the mechanisms by which microRNAs and lactobacilli exert their beneficial effects on intestinal epithelial permeability. Hence, to elucidate whether miRNAs and lactobacilli play roles in intestinal epithelial barrier regulation, we compared miRNA expression levels in intestinal epithelial cells (IECs) under Lactobacillus casei ( L. casei LC01) treatment. IECs and L. casei LC01 were co-cultured and then subjected to microRNA microarray assay. qRT-PCR, western blot and ELISA were used to detect the expression of occludin (OCLN) and zonula occludens 1 (ZO1/TJP1). The interaction between miRNAs and L. casei LC01 acting in IECs was investigated through transfection of RNA oligoribonucleotides and pcDNA 3.1 plasmid. The results are as follows: 1) L. casei LC01 decreased the expression of miR-144 and FD4 and promoted OCLN and ZO1 expression in IECs; 2) L. casei LC01 enhanced the barrier function of IECs via downregulation of miR-144 and upregulation of OCLN and ZO1; 3) Under L. casei LC01 treatment, OCLN and ZO1 overexpression could partially eliminate the promoting effect of miR-144 on intestinal permeability in IECs. Our results demonstrate that L. casei LC01 regulates intestinal permeability of IECs through miR-144 targeting of OCLN and ZO1. L. casei LC01 can be a possible therapeutic target for managing dysfunction of the intestinal epithelial barrier.

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Section: Discussionmentioning

confidence: 99%

Lactobacillus casei LC01 Regulates Intestinal Epithelial Permeability through miR-144 Targeting of OCLN and ZO1

Hou

Huang

Wang

et al. 2020

J. Microbiol. Biotechnol.

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“…Aspirin was shown to cause damage in the gastric system in a rat model by decreasing the plasma membrane protein of tight junctions, occludin expression, which was reversed by pretreatment with another drug mosapride. 17 High-dose of ibuprofen caused jejunal perforations even in short-courses. 18 Another anti-inflammatory drug, naproxen, causes gastric antral ulcerations, and an increase of lipid peroxide levels, but the effect was reversed with curcumin.…”

Section: Current Targets and Their Limitationsmentioning

confidence: 99%

Overview on the Discovery and Development of Anti-Inflammatory Drugs: Should the Focus Be on Synthesis or Degradation of PGE2?

Mahesh¹,

Kumar²,

Reddanna³

2021

JIR

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Inflammation is a protective response that develops against tissue injury and infection. Chronic inflammation, on the other hand, is the key player in the pathogenesis of many inflammatory disorders including cancer. The cytokine storm, an inflammatory response flaring out of control, is mostly responsible for the mortality in COVID-19 patients. Anti-inflammatory drugs inhibit cyclooxygenases (COX), which are involved in the biosynthesis of prostaglandins that promote inflammation. The conventional non-steroidal anti-inflammatory drugs (NSAIDs) are associated with gastric and renal side-effects, as they inhibit both the constitutive COX-1 and the inducible COX-2. The majority of selective COX-2 inhibitors (COXIBs) are without gastric side-effects but are associated with cardiac side-effects on long-term use. The search for anti-inflammatory drugs without side-effects, therefore, has become a dream and ongoing effort of the Pharma companies. As PGE 2 is the key mediator of inflammatory disorders, coming up with a strategy to reduce the levels of PGE 2 alone without affecting other metabolites may form a better choice for the development of next generation anti-inflammatory drugs. In this direction the options being explored are on synthesis of PGE 2 -mPGES-1; PGE 2 degradation through a specific PG dehydrogenase, 15-PGDH, and by blocking its activity mediated through a specific PGE receptor, EP4. As leukotrienes formed via the 5-lipoxygenase (5-LOX) pathway also play an important role in the mediation of inflammation, efforts are also being made to target both COX and LOX pathways. This review focuses on addressing the following three points: 1) How NSAIDs and COXIBs are associated with gastric, renal and cardiac side-effects; 2) Should the focus be on the targets upstream or downstream of PGE 2 ; and 3) the status of alternative targets being explored for the discovery and development of anti-inflammatory drugs without side-effects.

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“…Cells in the groups were treated with Codonopsis decoction subsequently cultured at 37˚C for 24 h. Following this, 10 µL of MTT solution (5 mg/mL; Sigma-Aldrich; Merck KGaA) was added to each well and incubated at 37 ˚C for 4 h. The culture medium was removed, dimethylsulfoxide (DMSO, Sigma-Aldrich; Merck KGaA) was added to each well and cells were incubated at 37˚C for 10 min, following which the absorbance (A) of MTT was measured at 490 nm using a microplate reader (Bio-Rad Laboratories, Inc., Hercules, CA, USA). According to the above test results: cells were subsequently divided into control group (1640 only), positive control group (3.3 mg/mL aspirin +10 mg/mL OME), aspirin injury group (3.3 mg/ mL) and Codonopsis decoction groups (3.3 mg/mL aspirin + 0.05, 0.1 and 0.2 mg/mL Codonopsis decoction) [14]. Cells in the groups were treated with aspirin or Codonopsis decoction subsequently cultured at 37˚C for 12 and 24 h. All experiments were repeated 3 times.…”

Section: Mtt Assaymentioning

confidence: 99%

Codonopsis Decoction Inhibits Aspirin-Induced Gastric Mucosal Injury in Rats by Regulating COX, COX-1, COX-2, TNF-α, IL-6 and TGF-α

Wang¹,

Lu²,

Deng³

et al. 2021

BJSTR

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Codonopsis (Codonopsis pilosula (Franch.) Nannf.) is a common medicinal and edible plant with a variety of biological functions, including enhancing gastrointestinal motility, anti-inflammatory, antioxidant, regulating glucose and lipid metabolism, regulating immune response and anti-tumor. Aspirin is a widely used clinical drug with multiple therapeutic effects. However, long-term use of aspirin could also bring some side effects, including gastrointestinal discomfort, liver and kidney damage, asthma, and allergies. The present study is aimed to investigate the effect of Codonopsis decoction on aspirin-induced gastric injuries. Cell proliferation was evaluated by MTT assay and cell apoptosis was investigated by flow cytometry. Gastric mucosal injury index and HE staining were used to evaluate the pathological changes of gastric tissue. The levels of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and transforming growth factor-α (TGF-α) in GES-1 cells culture supernatant were detected by ELISA kits. The levels of cyclooxygenase (COX), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and TGF-α in gastric tissue and serum were detected by ELISA kits. Results showed that Codonopsis decoction significantly attenuated the aspirin-induced cytotoxicity and apoptosis of GES-1 cells. Codonopsis decoction significantly increased the levels of COX-1, COX-2 and TGF-α in GES-1 cells treated by aspirin. Codonopsis decoction could also increase the expression levels of COX and TGF-α in vivo. Codonopsis decoction significantly reduced the levels of TNF-α and IL-6 both in vivo and in vitro. In addition, Codonopsis decoction could increase the daily weight gain of rats taking aspirin, and significantly reduce the gastric tissue damage and gastric mucosal injury index. These data indicated that Codonopsis decoction may possess potential to reduce the side effects caused by oral aspirin and may help the safe use of aspirin.

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Increased expression of tight junction proteinï¿½occludin is associated with the protective effect of mosapride against aspirin‑induced gastric injury

Cited by 7 publications

References 26 publications

Lactobacillus casei LC01 Regulates Intestinal Epithelial Permeability through miR-144 Targeting of OCLN and ZO1

Lactobacillus casei LC01 Regulates Intestinal Epithelial Permeability through miR-144 Targeting of OCLN and ZO1

Overview on the Discovery and Development of Anti-Inflammatory Drugs: Should the Focus Be on Synthesis or Degradation of PGE2?

Codonopsis Decoction Inhibits Aspirin-Induced Gastric Mucosal Injury in Rats by Regulating COX, COX-1, COX-2, TNF-α, IL-6 and TGF-α

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