Chlorogenic Acid Suppresses miR‐155 and Ameliorates Ulcerative Colitis through the NF‐κB/NLRP3 Inflammasome Pathway

Zeng, Junhao; Zhang, Dengqing; Wang, Xiaoyu; Bai, Yuanling; Yuan, Chengfu; Wang, Ting; Yuan, Ding; Zhang, Changcheng; Liu, Chaoqi

doi:10.1002/mnfr.202000452

Cited by 55 publications

(40 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…UC is a common intestinal bowel disease characterized by intestinal epithelial injury, including extensive epithelial cell death, mucosal erosion, ulceration, and crypt abscess formation ( Lu et al, 2020 ; Wang et al, 2020 ). Several signaling pathways, including the NF-κB/NLRP3 inflammasome pathway ( Zeng et al, 2020 ), RIPK pathways ( Garcia-Carbonell et al, 2019 ), and the JAK/STAT pathway ( Zundler and Neurath, 2016 ), contribute to disease progression. In this study, we found that ghrelin could protect intestinal barrier in the colitis model induced by DSS via the UPR pathway.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin Inhibits Intestinal Epithelial Cell Apoptosis Through the Unfolded Protein Response Pathway in Ulcerative Colitis

et al. 2021

View full text Add to dashboard Cite

Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) that occurs in the lining of the rectum and colon. Apoptosis of the intestinal epithelial cells (IECs) is common in active UC patients. Ghrelin is reported to be downregulated in apoptosis of IECs induced by tumor necrosis factor-α (TNF-α). Therefore, we hypothesized that ghrelin might play an antiapoptotic role in UC progression, which was investigated using in vitro and in vivo studies. The TNF-α-treated Caco-2 cell model and mouse colitis model induced by dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzenesulfonic acid (TNBS) were established and employed. We found that ghrelin could inhibit the apoptosis of Caco-2 cells induced by TNF-α, which could be disturbed by [D-lys3]-GHRP-6, the antagonist of ghrelin receptor GHS-R1a. Similarly, in the DSS- and TNBS-induced mouse colitis models, ghrelin could also protect intestinal tissues from apoptosis in DSS- and TNBS-induced colitis depending on GHS-R1a. Furthermore, ghrelin modulated the unfolded protein response (UPR) pathway and regulated the expressions of caspase-3, BAX, and Bcl-2, which contributed to the inhibition of cell apoptosis. In conclusion, ghrelin protects IECs from apoptosis during the pathogenesis of colitis by regulating the UPR pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Ghrelin Inhibits Intestinal Epithelial Cell Apoptosis Through the Unfolded Protein Response Pathway in Ulcerative Colitis

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Chlorogenic Acid (31) Antimicrobial [125], hepatoprotective [126], antihypertensive, vasodilator [127], antitumor [129], anti-inflammatory [130], improves late diabetes [131], protects against cholestatic liver injury [132], neuroprotective [133], antiviral activity against influenza A (H1N1/H3N2) virus [134], anti-diabetic and anti-lipidemic [135], inhibits hepatocellular carcinoma [136], anxiolytic and antioxidant [137], antihyperalgesic [138], cardioprotective [139], neuroprotective and cognitive improvement [140], improves hepatic steatosis and insulin resistance [141], alleviates obesity and modulates gut microbiota [142], ameliorates ulcerative colitis [143], inhibits glioblastoma growth [144], induces 4T1 breast cancer tumor's apoptosis [145], strong matrix metalloproteinase-9 inhibitor [146].…”

Section: Secondary Metabolite Biological Activitiesmentioning

confidence: 99%

Next Chapter in the Legend of Silphion: Preliminary Morphological, Chemical, Biological and Pharmacological Evaluations, Initial Conservation Studies, and Reassessment of the Regional Extinction Event

Miski

2021

Plants

View full text Add to dashboard Cite

Silphion was an ancient medicinal gum-resin; most likely obtained from a Ferula species growing in the Cyrene region of Libya ca. 2500 years ago. Due to its therapeutic properties and culinary value, silphion became the main economic commodity of the Cyrene region. It is generally believed that the source of silphion became extinct in the first century AD. However, there are a few references in the literature about the cultivated silphion plant and its existence up to the fifth century. Recently, a rare and endemic Ferula species that produces a pleasant-smelling gum-resin was found in three locations near formerly Greek villages in Anatolia. Morphologic features of this species closely resemble silphion, as it appears in the numismatic figures of antique Cyrenaic coins, and conform to descriptions by ancient authors. Initial chemical and pharmacological investigations of this species have confirmed the medicinal and spice-like quality of its gum-resin supporting a connection with the long-lost silphion. A preliminary conservation study has been initiated at the growth site of this rare endemic Ferula species. The results of this study and their implications on the regional extinction event, and future development of this species will be discussed.

show abstract

“…The oncomiR-31 inhibits the translation of RAS P21 protein activator 1, an inhibitor of KRAS protooncogene, thus stimulating the transcription of the KRAS oncogene, which promotes cell cycle progression in colon cancer cells ( 32 ). According to previous research, miR-31, and other miRNAs such as miR155 ( 33 ) and miR144-3p ( 34 ), are modulated by CGA ( Fig. 5 ).…”

Section: Discussionmentioning

confidence: 69%

Gold nanoparticles enhance microRNA 31 detection in colon cancer cells after inhibition with chlorogenic acid

Luque-Badillo
¹
,

Hernandez-Tapia
²
,

Ramirez-Castillo
³

et al. 2021

Oncol Lett

7
0
5
0

View full text Add to dashboard Cite

In the present study, the inhibitory effect of chlorogenic acid (CGA), a phenolic compound with potential antitumor effects, on circulating microRNA 31 (miR-31), was evaluated in RKO colon cancer cells. The capacity of gold nanoparticles (AuNPs) to enhance miR-31 quantification after treatment with CGA was assessed. RKO cells were treated with different concentrations of CGA for 24, 48 and 72 h, after which AuNPs coupled to CD81 were added to the supernatants. Total RNA was extracted, and miR-31 was quantified by reverse transcription-quantitative PCR. The results revealed an 85% decrease in miR-31 level following treatment with 1,000 µM CGA for 72 h, and the highest capacity to detect miR-31 (after treatment and isolation with AuNPs + CD81) was observed at 24 h. Furthermore, CGA decreased the expression of the miR-31 oncogene in an in vitro colon cancer model, and the use of AuNPs enhanced the levels of miRNA detection. The results suggest that miR-31 inhibition is one mechanism by which CGA decreases colon cancer cell proliferation. Moreover, AuNPs can increase the capacity of miR-31 quantification, representing a new strategy to develop non-invasive tools for the molecular diagnosis and monitoring of colon cancer.

show abstract

Chlorogenic Acid Suppresses miR‐155 and Ameliorates Ulcerative Colitis through the NF‐κB/NLRP3 Inflammasome Pathway

Cited by 55 publications

References 40 publications

Ghrelin Inhibits Intestinal Epithelial Cell Apoptosis Through the Unfolded Protein Response Pathway in Ulcerative Colitis

Ghrelin Inhibits Intestinal Epithelial Cell Apoptosis Through the Unfolded Protein Response Pathway in Ulcerative Colitis

Next Chapter in the Legend of Silphion: Preliminary Morphological, Chemical, Biological and Pharmacological Evaluations, Initial Conservation Studies, and Reassessment of the Regional Extinction Event

Gold nanoparticles enhance microRNA 31 detection in colon cancer cells after inhibition with chlorogenic acid

Contact Info

Product

Resources

About