Silencing interleukin 1α underlies a novel inhibitory role of miR‐181c‐5p in alleviating low‐grade inflammation of rats with irritable bowel syndrome

Ji, Li‐Jiang; Li, Fang; Zhao, Ping; Weng, Li-Ping; Wei, Jun; Yan, Jing; Liu, Lina

doi:10.1002/jcb.28794

Cited by 15 publications

(9 citation statements)

References 42 publications

(89 reference statements)

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“…Wu et al revealed that miRNAs are dysregulated in chronic inflammatory bowel diseases, including ulcerative colitis, IBS, and infectious colitis ( 46 ). A previous study found that in IBS rats, miR-181c-5p expression was downregulated, while interleukin-1 alpha (IL-1α) expression was concurrently upregulated ( 47 ). Functionally, miR-181c-5p overexpression represses low-grade intestinal inflammation by inhibiting IL-1α expression in IBS rats ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-155-5p inhibition alleviates irritable bowel syndrome by increasing claudin-1 and ZO-1 expression

Guo¹,

Rao²,

Jiang³

et al. 2023

Ann Transl Med

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Background: Irritable bowel syndrome (IBS) is a common gastrointestinal disease. Emerging studies have demonstrated that microRNAs (miRNAs) are commonly dysregulated in patients with IBS, and aberrant miRNAs are implicated in IBS occurrence. Although miR-155-5p participates in inflammatory bowel disease (IBD) and intestinal barrier dysfunction, the role of miR-155-5p in IBS is unclear.Methods: In the present study, colon samples were obtained from IBS patients and IBS mice induced by trinitrobenzenesulfonic acid (TNBS), and the levels of miR-155-5p, claudin-1 (CLDN1), and zonula occludens-1 (ZO-1) were assessed using real-time polymerase chain reaction (qRT-PCR) and immunohistochemical analysis. The regulatory role of miR-155-5p in CLDN1 and ZO-1 expression was validated using dual luciferase reporter assay.Results: We found that miR-155-5p levels were upregulated in colon samples of IBS patients and mice compared with healthy subjects and normal mice, respectively. Meanwhile, the levels of CLDN1 and ZO-1 were decreased in colon samples of IBS patients and mice. Importantly, forced expression of miR-155-5p inhibited CLDN1 and ZO-1 expression. In IBS mice, intraperitoneal injection with miR-155-5p inhibitor increased CLDN1 and ZO-1 expression in intestinal mucosal epithelium, enhanced visceral response thresholds, and decreased myeloperoxidase (MPO) activity.Conclusions: In summary, these results suggested that miR-155-5p participated in the pathogenesis of IBS, at least in part by inhibiting CLDN1 and ZO 1 expression, indicating that miR-155-5p may be a potential therapeutic target for IBS.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-155-5p inhibition alleviates irritable bowel syndrome by increasing claudin-1 and ZO-1 expression

Guo¹,

Rao²,

Jiang³

et al. 2023

Ann Transl Med

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“…M miR-181c-5p mimic; MC miR-181c-5p mimic control; ELISA enzyme linked immunosorbent assay; qRT-PCR quantitative reverse transcription real time polymerase chain reaction MiR-181c-5p can increase the production of malondialdehyde and reactive oxygen species, promote the apoptosis of HUVECs, and significantly enhance high glucose-induced oxidative stress damage (Shen et al 2018). Overexpressed miR-181c-5p inhibits the inflammatory response in rats with irritable bowel syndrome by silencing IL1A (Ji et al 2019). The inconsistent function of miR-181c-5p on apoptosis might depend on different cells and mechanisms, which needs further research.…”

Section: Discussionmentioning

confidence: 99%

CircPTK2-miR-181c-5p-HMGB1: a new regulatory pathway for microglia activation and hippocampal neuronal apoptosis induced by sepsis

Peng

et al. 2021

Mol Med

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Background Circular RNA hsa_circ_0008305 (circPTK2), miR-181c-5p and High mobility group box-1 (HMGB1) had a targeted regulatory relationship through bioinformatics analysis. This study explained the effects of these genes in microglia and sepsis mice. Methods Lipopolysaccharide (LPS) or Cecal Ligation and Puncture (CLP) was used to induce inflammation cell model or sepsis mouse model, as needed. Gene levels were measured by enzyme linked immunosorbent assay (ELISA), quantitative real-time PCR or Western blot, as required. Apoptosis was detected by TUNEL assay, and RNase R was used to test the stability of circPTK2. Targeting relationships between genes were analyzed using bioinformatics analysis and dual luciferase assay. Morris water maze test and mitochondrial membrane potential (MMP) detection were conducted to analyze the effects of genes on cognitive dysfunction of mice. Results Lipopolysaccharide induction triggered the release of pro-inflammatory cytokines, the upregulation of HMGB1 and circPTK2, and the downregulation of miR-181c-5p in microglia. Overexpression of HMGB1 enhanced the effect of LPS, while silencing HMGB1 partially counteracted the effect of LPS. Moreover, miR-181c-5p was a target of circPTK2 and bound to HMGB1. MiR-181c-5p mimic partially reversed the functions of LPS and HMGB1 overexpression, reduced the levels of TNF-α, IL-1β, and HMGB1, and inhibited apoptosis. CircPTK2 knockdown had the same effect as miR-181c-5p up-regulation. In vivo, sicircPTK2 improved cognitive function, restored MMP level, inhibited apoptosis, reduced the levels of inflammatory factors and apoptotic factors, and increased the survival rate of CLP-induced mice. Conclusion Our research reveals that circPTK2 regulates microglia activation and hippocampal neuronal apoptosis induced by sepsis via miR-181c-5p-HMGB1 signaling.

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“…The procedure was repeated for three times for each rat, and the average value of the three times was taken. The scoring standard was conducted according to the previous study [ 26 ].…”

Section: Methodsmentioning

confidence: 99%

Effect of local ozone treatment on rats with anterior rectal resection and the possible mechanisms

Zhang

Chen

et al. 2021

BioMed Eng OnLine

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Background Anterior resection syndrome (ARS) is characterized by the diverse and interchangeable evacuatory symptoms that may occur following distal colorectal resection. We aimed to investigate the effect and potential mechanisms of ozone perfusion on rats with anterior rectal resection (ARR). Material and methods After establishment of rat ARR model, 20, 40 and 80 ug/ml ozone was used to treat rats by enema administration. The pathological examination of intestinal tissue was detected using hematoxylin–eosin staining. The rate of loose stools, minimum threshold volume of abdominal withdrawal reflex (AWR) and Bristol grade were used to evaluate the degree of abnormal defecation function. Subsequently, the levels of oxidative stress- and inflammation-related markers, 5-hydroxytryptamine (5-HT), inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in the serum and intestinal tissue were determined with the corresponding kits. Meanwhile, the expression of nuclear factor kappa B (NF-κB) p65, transient receptor potential vanilloid (TRPV)1, TRPV4, iNOS and 5-HT receptor 3A (5-HTR3A) was determined with RT-qPCR and western blotting. Results Ozone administration (20 and 40 ug/ml) significantly alleviated the pathological changes of intestinal tissue-induced by ARR, accompanied by the decreased loose stools rate, Bristol score and increased abdominal withdraw reflex. However, 80 ug/ml of ozone intervention played opposite roles in the aforementioned changes with 20 and 40 ug/ml of ozone. Additionally, remarkably elevated reactive oxygen species (ROS), malonaldehyde (MDA), superoxide dismutase (SOD), 5-HT, iNOS and NO levels were observed in the ozone-treated groups (20 and 40 ug/ml), while high dose of ozone drastically improved ROS, MDA, 5-HT, iNOS and NO levels but reduced the activity of SOD. Consistently, the contents of inflammatory factors were decreased after low and middle doses of ozone administration. However, high dose of ozone aggravated the inflammatory injury. Moreover, 20 and 40 ug/ml ozone upregulated TRPV1 and TRPV4 expression but downregulated 5-HTR3A expression, which was restored after 80 ug/ml of ozone intervention. Remarkably, the levels of NF-κB p65 and iNOS were dose-dependently enhanced following ozone treatment. Conclusions Taken together, low concentration of ozone attenuated intestinal injury induced by ARR via balancing oxidative stress and inflammation, but high concentration of ozone exacerbated the intestinal injury, which might be related to the 5-HT and TRPV signaling.

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Silencing interleukin 1α underlies a novel inhibitory role of miR‐181c‐5p in alleviating low‐grade inflammation of rats with irritable bowel syndrome

Cited by 15 publications

References 42 publications

MicroRNA-155-5p inhibition alleviates irritable bowel syndrome by increasing claudin-1 and ZO-1 expression

MicroRNA-155-5p inhibition alleviates irritable bowel syndrome by increasing claudin-1 and ZO-1 expression

CircPTK2-miR-181c-5p-HMGB1: a new regulatory pathway for microglia activation and hippocampal neuronal apoptosis induced by sepsis

Effect of local ozone treatment on rats with anterior rectal resection and the possible mechanisms

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