Activation of sirtuin 1 by catalpol-induced down-regulation of microRNA-132 attenuates endoplasmic reticulum stress in colitis

Xiong, Yongjian; Shi, Liqiang; Wang, Liang; Zhou, Zijuan; Wang, Chenou; Lin, Yuan; Luo, Dong; Chen, Dapeng

doi:10.1016/j.phrs.2017.05.030

Cited by 42 publications

(32 citation statements)

References 33 publications

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“…Recently, the inhibited effect on inflammation and tumor angiogenesis of catalpol in CRC cells was revealed and catalpol was considered as a potential candidate compound for treating CRC (3,10,20). Significant changes in the miRNA expression profiles were observed in cancer cells after catalpol treatment (8)(9)(10)21). Moreover, the present findings indicated that miR-34a played a tumor-suppressive role during progression of human CRC and cholangiocarcinoma (11,12).…”

Section: Discussionsupporting

confidence: 51%

“…Moreover, the antitumor effects of catalpol were neutralized by concurrent silencing of miR-34a expression. Previous studies indicated that catalpol administration significantly alleviated symptoms in a rat colitis model (21,29). The present results indicated that there was no significant weight gain in any of the experimental groups, which may be because the experiment period was not long enough.…”

Section: Discussioncontrasting

confidence: 46%

“…Mounting evidence has revealed that catalpol has inhibitory effects on proliferation and inducing effects on apoptosis in several types of human malignancies (8)(9)(10)21). Moreover, catalpol was revealed to inhibit autophagy and decrease apoptosis via the mammalian target of rapamycin pathway in denervated muscular atrophy (16).…”

Section: Discussionmentioning

confidence: 99%

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Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer

2020

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Colorectal cancer (CRC) is one of the most common digestive tract tumors worldwide. Catalpol exerts inhibitory effects on the progression of several cancer types by regulating microRNAs (miRs). However, the precise role and carcinostatic mechanism of catalpol on CRC cells are poorly understood which limits the application of catalpol treatment. In the present study, miR-34a and sirtuin 1 (SIRT1) expression levels were detected in CRC tissues and CRC cell lines by RT-qPCR. Computational software analysis, luciferase assays and western blotting were used to demonstrate the downstream target of miR-34a in CRC cells. Effects of catalpol on cell viability, apoptosis, autophagic flux and the miR-34a/SIRT1 axis in the CRC cells were assessed by CCK-8 assay, flow cytometry, electron microscopy and western blotting, respectively. Whether the miR-34a/SIRT1 axis participated in catalpol-mediated autophagy and apoptosis was investigated. The effects of catalpol on the miR-34a/SIRT1 axis and malignant behavior were evaluated in a rat model of azoxymethane (AOM)-induced CRC. It was revealed that miR-34a expression levels were significantly decreased while SIRT1 was overexpressed in most of the CRC tissues and all the CRC cell lines. Clinically, a low level of miR-34a was correlated with poor clinicopathological characteristics in CRC patients. Catalpol reduced cell viability, suppressed autophagy, promoted apoptosis, and regulated the expression of SIRT1 by inducing miR-34a in vitro and in vivo. The autophagy-inhibiting effect of catalpol may be a mechanism to promote apoptosis of CRC cells. miR-34a mimic transfection resulted in autophagy-suppressive activity similar to that of catalpol, while the miR-34a inhibitor attenuated the antiautophagic effects of catalpol. In conclusion, miR-34a is involved in regulating catalpol-mediated autophagy and malignant behavior by directly inhibiting SIRT1 in CRC.

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Section: Discussionsupporting

confidence: 51%

Section: Discussioncontrasting

confidence: 46%

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Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer

2020

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“…Although few epidemiological studies and intervention trials are available, experiments conducted on cell cultures or in animals have established that some of these phytochemicals deliver at least some of their antioxidant, anti-inflammatory and/or anti-proliferative effects through the modification of the composition of endogenous microRNA populations. For example, catalpol, an iridoid glucoside found in plants of genus Rehmannia , has been shown to reduce endoplasmic reticulum stress in UC through the down-regulation of miR-132 [58], while salvianolic acid B, extracted from Salvia miltiorrhiza , restored impaired IB in a rat model of TNBS-induced colitis likely through inducing downregulation of MLCK by miR-1 [59]. Also, flavonoid and non-flavonoid poly-phenols found in different fruits and berries present antioxidant, anti-inflammatory and/or anti-proliferative effects on cell cultures or in murine models, including cases of gut inflammation or colon cancer.…”

Section: Resultsmentioning

confidence: 99%

MicroRNAs in intestinal barrier function, inflammatory bowel disease and related cancers — their effects and therapeutic potentials

Tili

Michaille

Piurowski

et al. 2017

Current Opinion in Pharmacology

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The initiation and development or inflammatory bowel disease (IBD) and associated colorectal cancers, have been linked to inflammation. MicroRNAs are non-coding regulators of gene expression that have gained great attention due to their capability to regulate the expression of a number of target transcripts. It is now generally admitted that microRNAs are instrumental in gut pathologies, in particular through their targeting of transcripts encoding proteins of the intestinal barrier (IB) and their regulators. Intense research is conducted to identify microRNAs susceptible to be used as biomarkers and to design new therapeutic approaches based upon using synthetic microRNA mimics and inhibitors as well as finding new drugs capable to restore or modify microRNA expression in the context of gut pathologies.

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“…S1, † is an iridoid glucoside and has been found to be present in large quantities in the root of Romania glutinosa L. 12 As a traditional medicine, catalpol demonstrates a variety of biological activities including anticancer, neuro-protective, anti-inammatory, diuretic, hypoglycemic and anti-hepatitis virus effects. 17,18 Previous studies have also provided some clues that catalpol can affect energy metabolism through increasing mitochondrial biogenesis, enhancing endogenous antioxidant enzymatic activities and inhibiting free radical generation. 19,20 What's more, recent studies provided that catalpol could up-regulate the decreased AMPK phosphorylation in db/db mice and ameliorate high-fat diet-induced adipose tissue inammation by suppressing NF-kB.…”

Section: 2mentioning

confidence: 99%

Catalpol attenuates oxidative stress and promotes autophagy in TNF-α-exposed HAECs by up-regulating AMPK

et al. 2017

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Oxidative stress and autophagy dysfunction are critical factors in the pathogenesis of atherosclerosis. Adenosine 50 monophosphate-activated protein kinase (AMPK) plays an important role in inhibiting oxidative stress and promoting autophagy. Catalpol, an iridoid glucoside extracted from the root of Rehmanniae glutinosa L, was reported to produce a potent antioxidant effect. However, the mechanism of catalpol inhibiting oxidative stress and its effect on AMPK remain unclear. This study aims to investigate the potential role of catalpol in regulating oxidative stress and autophagy in tumor necrosis factor-a (TNF-a)-treated human aorta epithelial cells (HAECs), and the important role of AMPK involved in catalpol's effects. In the present study, effects of catalpol on inhibiting oxidative stress and the related adhesion, apoptosis and promotion of autophagy were demonstrated. Catalpol also produces a potent effect on activating AMPK in TNF-a-treated HAECs. Mechanistically, the effects of catalpol on inhibiting oxidative stress and increasing the autophagy level were partly blocked by a pharmacological AMPK inhibitor, compound C or AMPK small interfering RNA, indicating that catalpol performed such protective effects by activating AMPK. In summary, this study demonstrated that AMPK is a key treatment target for endothelial cell injury and catalpol confers protection on TNF-a-treated HAECs by up-regulating AMPK activity. Catalpol has highly favorable characteristics for the treatment of atherosclerosis.

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Activation of sirtuin 1 by catalpol-induced down-regulation of microRNA-132 attenuates endoplasmic reticulum stress in colitis

Cited by 42 publications

References 33 publications

Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer

Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer

MicroRNAs in intestinal barrier function, inflammatory bowel disease and related cancers — their effects and therapeutic potentials

Catalpol attenuates oxidative stress and promotes autophagy in TNF-α-exposed HAECs by up-regulating AMPK

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