Suppression of miR-21 and miR-155 of macrophage by cinnamaldehyde ameliorates ulcerative colitis

Qu, Shulan; Shen, Yunhui; Wang, Mengjie; Wang, Xiaoyu; Yang, Ye

doi:10.1016/j.intimp.2018.11.045

Cited by 60 publications

(60 citation statements)

References 36 publications

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“…Formononetin was described to promote the expression of epithelial cell tight junctions, which are prominently reduced in DSS-induced colitis, and maintained the colonic epithelial barrier [75]. Cinnamaldehyde was described to ameliorate ulcerative colitis through the suppression of miR-21 and miR-155 in the colon and macrophage [76].…”

Section: The Nlrp3 Inflammasome and Ibdmentioning

confidence: 99%

Does NLRP3 Inflammasome and Aryl Hydrocarbon Receptor Play an Interlinked Role in Bowel Inflammation and Colitis-Associated Colorectal Cancer?

2020

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Inflammation is a hallmark in many forms of cancer; with colitis-associated colorectal cancer (CAC) being a progressive intestinal inflammation due to inflammatory bowel disease (IBD). While this is an exemplification of the negatives of inflammation, it is just as crucial to have some degree of the inflammatory process to maintain a healthy immune system. A pivotal component in the maintenance of such intestinal homeostasis is the innate immunity component, inflammasomes. Inflammasomes are large, cytosolic protein complexes formed following stimulation of microbial and stress signals that lead to the expression of pro-inflammatory cytokines. The NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been extensively studied in part due to its strong association with colitis and CAC. The aryl hydrocarbon receptor (AhR) has recently been acknowledged for its connection to the immune system aside from its role as an environmental sensor. AhR has been described to play a role in the inhibition of the NLRP3 inflammasome activation pathway. This review will summarise the signalling pathways of both the NLRP3 inflammasome and AhR; as well as new-found links between these two signalling pathways in intestinal immunity and some potential therapeutic agents that have been found to take advantage of this link in the treatment of colitis and CAC.

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Section: The Nlrp3 Inflammasome and Ibdmentioning

confidence: 99%

Does NLRP3 Inflammasome and Aryl Hydrocarbon Receptor Play an Interlinked Role in Bowel Inflammation and Colitis-Associated Colorectal Cancer?

2020

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“…Moreover, levels of reactive oxygen species were also reduced, along with the phosphorylation of AKT, mTOR, and COX2 proteins. Further experiments revealed similar suppression of IL-1β and IL-6 in response to miR-21 or miR-155 inhibitors, demonstrating that these inflammatory factors are positively regulated by miR-21 or miR-155 (Qu et al, 2018). As a result, CA suppresses the miR-21/miR-155/IL-1β/IL-6 axis to exert its protective function in ulcerative colitis.…”

Section: Anti-inflammatory Effects Of Chmsmentioning

confidence: 83%

“…Some miRNAs, including miR-21, miR-34a, miR-34c, miR-155, miR-29a, miR-203, miR-27b, miR-184, and miR-143, contributed to the treatment mechanisms of more than one bioactive ingredient of CHMs. In particular, miR-21 was identified as targeted and regulated by BBR (Luo et al, 2014), TP (Li et al, 2016), RES (Wang G. et al, 2015), CA (Qu et al, 2018), ICA (Li J. et al, 2015), AIL (Yang P. et al, 2018), Car/Thy (Khosravi and Erle, 2016), DHM (Yang D. et al, 2018), and COR (Yang et al, 2017), especially in its anti-cancer activities, indicating that this miRNA is stably targetable and responsive to the pharmacological effects of various CHMs. Moreover, miR-155 was associated with inflammatory responses and could be inhibited by CUR, RES, Tan IIA, CA, Car/Thy and AKBA, in inflammatory-related diseases (Tili et al, 2010; Fan et al, 2016; Khosravi and Erle, 2016; Ma F. et al, 2017; Xuan et al, 2017; Qu et al, 2018; Sayed et al, 2018).…”

Section: Resultsmentioning

confidence: 99%

“…According to TCM theory, the traditional plant can enhance the function of “yang qi” (a substance with excitatory function in TCM) and is often used to relieve symptoms of weakness. Recent studies have broadened the application of this preparation to the treatment of cerebrovascular diseases, ulcerative colitis, and cancer (Zhao et al, 2015; Tian F. et al, 2017; Qu et al, 2018), where it acts by exerting anti-inflammatory or ncRNA regulatory functions. CA improves symptoms of weight loss, disease activity index, and infiltration of inflammatory cells, by decreasing the levels of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, as well as the NLRP3 inflammasome, miR-21, and miR-155, in both colon tissue and macrophages.…”

Section: Anti-inflammatory Effects Of Chmsmentioning

confidence: 99%

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Bioactive Ingredients in Chinese Herbal Medicines That Target Non-coding RNAs: Promising New Choices for Disease Treatment

et al. 2019

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Chinese herbal medicines (CHMs) are widely used in China and have long been a powerful method to treat diseases in Chinese people. Bioactive ingredients are the main components extracted from herbs that have therapeutic properties. Since artemisinin was discovered to inhibit malaria by Nobel laureate Youyou Tu, extracts from natural plants, particularly bioactive ingredients, have aroused increasing attention among medical researchers. The bioactive ingredients of some CHMs have been found to target various non-coding RNA molecules (ncRNAs), especially miRNAs, lncRNAs, and circRNAs, which have emerged as new treatment targets in numerous diseases. Here we review the evidence that, by regulating the expression of ncRNAs, these ingredients exert protective effects, including pro-apoptosis, anti-proliferation and anti-migration, anti-inflammation, anti-atherosclerosis, anti-infection, anti-senescence, and suppression of structural remodeling. Consequently, they have potential as treatment agents in diseases such as cancer, cardiovascular disease, nervous system disease, inflammatory bowel disease, asthma, infectious diseases, and senescence-related diseases. Although research has been relatively limited and inadequate to date, the promising choices and new alternatives offered by bioactive ingredients for the treatment of the above diseases warrant serious investigation.

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“…Red (mCherry) fluorescence indicated autolysosomes and yellow fluorescence, due to merging of both green and red fluorescence, indicated autophagosomes. 14) Nitrite Assay The amount of nitric oxide (NO) was assessed by determining the nitrite concentration in the supernatant with Griess reagent according to the manufacturer's protocol.…”

Section: Methodsmentioning

confidence: 99%

Metformin Suppresses LPS-Induced Inflammatory Responses in Macrophage and Ameliorates Allergic Contact Dermatitis in Mice <i>via</i> Autophagy

Wang

et al. 2020

Biological & Pharmaceutical Bulletin

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Allergic contact dermatitis (ACD) is one of the most common skin diseases caused by hapten-modified proteins. Metformin, a drug commonly prescribed for type II diabetes, has been demonstrated to have various biological functions beyond its antidiabetic effects. However, its role in ACD remains unknown. In the present study, we found that metformin reduced the production of nitric oxide (NO) and the level of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. These anti-inflammatory effects were also demonstrated on bone marrow-derived macrophages (BMDMs). Furthermore, metformin also enhanced autophagic flux, inhibited the phosphorylation of the serine/threonine protein kinase (AKT)/mammalian target of rapamycin (mTOR), mitogen-activated protein kinases (MAPKs) related protein levels and the level of miR-221 in LPS-stimulated RAW264.7 cells. Besides, metformin attenuated 2,4-dinitrofluorobenzene (DNFB)-induced ACD and inhibited proinflammatory cytokines in the ear. In addition, metformin ameliorated ACD partly through the inhibition of macrophage activation and the induction of autophagic flux. Taken together, our data indicated that metformin ameliorates ACD through enhanced autophagic flux to inhibit macrophage activation and provides a potential contribution to ACD treatment.

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Suppression of miR-21 and miR-155 of macrophage by cinnamaldehyde ameliorates ulcerative colitis

Cited by 60 publications

References 36 publications

Does NLRP3 Inflammasome and Aryl Hydrocarbon Receptor Play an Interlinked Role in Bowel Inflammation and Colitis-Associated Colorectal Cancer?

Does NLRP3 Inflammasome and Aryl Hydrocarbon Receptor Play an Interlinked Role in Bowel Inflammation and Colitis-Associated Colorectal Cancer?

Bioactive Ingredients in Chinese Herbal Medicines That Target Non-coding RNAs: Promising New Choices for Disease Treatment

Metformin Suppresses LPS-Induced Inflammatory Responses in Macrophage and Ameliorates Allergic Contact Dermatitis in Mice <i>via</i> Autophagy

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