RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

Zhao, Qian; Liu, Yang; Tan, Lei; Yan, Liyong; Zuo, Xiuli

doi:10.1007/s00011-018-1155-6

Cited by 15 publications

(13 citation statements)

References 44 publications

(39 reference statements)

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“…In addition, infusion of osmotin using osmotic pumps attenuates dextran sodium sulfate-induced colitis in mice [58] . These effects are consistent with anti-inflammatory effects of adiponectin and AdipoRon [58][59][60] . The results from in vitro and in vivo experiments indicate that osmotin as well as adiponectin and AdipoRon could prevent inflammatory diseases.…”

Section: Anti-inflammatory Effectsupporting

confidence: 84%

Therapeutic properties of the new phytochemical osmotin for preventing atherosclerosis

Watanabe¹

2020

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Section: Anti-inflammatory Effectsupporting

confidence: 84%

Therapeutic properties of the new phytochemical osmotin for preventing atherosclerosis

Watanabe¹

2020

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“…57 DSSinduced colonic inflammation is commonly accompanied by apoptosis via influencing apoptosis-related proteins in response to various cellular stresses, such as inflammation and oxidative stress. 58 In addition, it has been reported that peripheral inflammation can induce neuroinflammation in the CNS via disruption of the BBB. 8 The unique characteristics of this barrier include tight intercellular junctions.…”

Section: Discussionmentioning

confidence: 99%

Effect of N‐palmitoylethanolamine‐oxazoline on comorbid neuropsychiatric disturbance associated with inflammatory bowel disease

et al. 2020

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Inflammatory bowel disease (IBD) is a chronic disorder characterized by inflammation of the gastrointestinal (GI) tract, and it is associated with different neurological disorders. Recent evidence has demonstrated that the gut‐brain‐axis has a central function in the perpetuation of IBS, and for this reason, it can be considered a possible therapeutic target. N‐Palmitoylethanolamine‐oxazoline (PEA‐OXA) possesses anti‐inflammatory and potent neuroprotective effects. Although recent studies have explained the neuroprotective properties of PEA‐OXA, nothing is known about its effects on the gut‐brain axis during colitis. The aim of this study is to explore the mechanism and the effect of PEA‐OXA on the gut‐brain axis in rats subjected to experimental colitis induced by oral administration of dextran sulfate sodium (DSS). Daily oral administration of PEA‐OXA (10 mg/kg daily o.s.) was able to decrease the body weight loss, macroscopic damage, colon length, histological alteration, and inflammation after DSS induction. Additionally, PEA‐OXA administration enhanced neurotrophic growth factor release and decreased the astroglial and microglial activation induced by DSS. Moreover, PEA‐OXA restored intestinal permeability and tight junctions (TJs) as well as reduced apoptosis in the colon and brain. In our work, we demonstrated, for the first time, the action of PEA‐OXA on the gut‐brain axis in a model of DSS‐induced colitis and its implication on the “secondary” effects associated with colonic disturbance.

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“…Therefore, the present study aimed to identify a novel target and to explore the underlying mechanisms for IBD treatment. DSS is widely adopted to stimulate colonic inflammation for in vivo and in vitro IBD models (25,26), and in a DSS mouse IBD model, DSS appears to be directly toxic to colonic epithelial cells in the basal crypt (26). Thus, in the present study, DSS was used to treat Caco-2 cells and the effects of DSS on Caco-2 cells and IBD tissues were examined.…”

Section: Discussionmentioning

confidence: 98%

Mechanism underlying the significant role of the miR‑4262/SIRT1 axis in children with inflammatory bowel disease

Deng

Shang

et al. 2020

Exp Ther Med

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Inflammatory bowel disease (IBD) is a term used to describe chronic and recurrent gastrointestinal disease. In total, >2 million individuals worldwide have been diagnosed with IBD, including ulcerative colitis (UC), Crohn's disease (CD) and indeterminate colitis. There is accumulating evidence to indicate that microRNAs (miRNAs or miRs) are involved in the development and progression of IBD. miR-4262, an underlying promoter in tumor diseases, has been reported to regulate inflammatory responses. However, the potential mechanisms underlying the role of miR-4262 in IBD remain unknown. The present study attempted to explore the role and mechanisms of miR-4262 in IBD. Firstly, reverse transcription-quantitative PCR (RT-qPCR) was used to detect the expression of miR-4262 in 30 IBD colonic mucosa tissues, 30 normal tissues, 2% dextran sulfate sodium (DSS)-treated Caco-2 cells and normal cells. It was demonstrated that the expression levels of miR-4262 in IBD colonic mucosa tissues and 2% DSS-stimulated Caco-2 cells were markedly higher compared with those in the control groups. Target gene prediction databases and dual-luciferase reporter assays were then used, and sirtuin 1 (SIRT1) was identified as a target gene of miR-4262. Furthermore, the levels of SIRT1 in 2% DSS-stimulated Caco-2 cells and IBD colonic mucosa tissues were suppressed compared with the corresponding control groups. In addition, it was observed that miR-4262 negatively regulated SIRT1 expression in Caco-2 cells. Thereafter, Caco-2 cells were treated with inhibitor control, miR-4262 inhibitor, control-siRNA or SIRT1-siRNA for 48 h, followed by 2% DSS treatment for 4 days. The secretion of inflammatory factors was analyzed via ELISA and RT-qPCR. MTT assay, flow cytometry and western blot analysis were performed to assess cell viability, apoptosis and NF-κB signaling pathway-related protein levels, respectively. The results indicated that DSS enhanced the inflammatory response, suppressed cell viability and promoted cell apoptosis, and this was decreased following transfection with an miR-4262 inhibitor. In addition, 2% DSS upregulated p-p65 expression and enhanced the ratio of p-p65/p65, while the miR-4246 inhibitor exerted an opposite effect. All the effects of miR-4262 inhibitor on Caco-2 cells were eliminated following transfection with SIRT1-siRNA. It was thus concluded that miR-4262 may serve a role in the progression of IBD via targeting SIRT1, and miR-4262/SIRT1 may represent a potential target for the diagnosis and treatment of IBD.

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RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

Cited by 15 publications

References 44 publications

Therapeutic properties of the new phytochemical osmotin for preventing atherosclerosis

Therapeutic properties of the new phytochemical osmotin for preventing atherosclerosis

Effect of N‐palmitoylethanolamine‐oxazoline on comorbid neuropsychiatric disturbance associated with inflammatory bowel disease

Mechanism underlying the significant role of the miR‑4262/SIRT1 axis in children with inflammatory bowel disease

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