Oral Concentrated Grape Juice Suppresses Expression of NF-kappa B, TNF-α and iNOS in Experimentally Induced Colorectal Carcinogenesis in Wistar Rats

Campanholo, Vanessa Maria de Lima Pazine; Silva, Roseane Mendes; Silva, Tiago Donizetti; Neto, Ricardo Artigiani; Paiotti, Ana Paula Ribeiro; Ribeiro, Daniel Araki; Forones, Nora Manoukian

doi:10.7314/apjcp.2015.16.3.947

Cited by 10 publications

(8 citation statements)

References 29 publications

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“…51 It has been evidenced that the risk of developing inflammatory bowel disease-associated CRC is highly correlated with the extension and duration of inflammation. 51 It has been evidenced that the risk of developing inflammatory bowel disease-associated CRC is highly correlated with the extension and duration of inflammation.…”

Section: Discussionmentioning

confidence: 99%

Crocin synergistically enhances the antiproliferative activity of 5‐flurouracil through Wnt/PI3K pathway in a mouse model of colitis‐associated colorectal cancer

Amerizadeh

Rezaei

Rahmani

et al. 2018

J of Cellular Biochemistry

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Colorectal cancer (CRC) is the third most common cause of cancer-related death, and hence there is a need for the identification of novel-agents to improve the efficacy of existing therapies. There is growing evidence for the antitumor activity of crocin, although its activity and molecular mechanisms in CRC remains to be elucidated. Here we explored the therapeutic application of crocin or its combination with 5-flurouracil in a mouse model of colitis-associated colon cancer. The antiproliferative activity of crocin was assessed in two-dimensional and three-dimensional cell-culture models. The migratory behaviors were determined, while the expression levels of several genes were assessed by quantitative reverse transcriptase polymerase chain reaction/Western blot analysis. We examined the anti-inflammatory properties of crocin by pathological evaluation and disease-activity index as well as oxidative or antioxidant markers: malondialdehyde (MDA) and total-thiols (T-SH) levels and superoxide dismutase (SOD) and catalase (CAT) activity. Crocin suppressed cell-growth and the invasive behavior of CRC cells through modulation of the Wnt-pathway and E-cadherin. Moreover, administration of crocin alone, or in combination with 5-FU dramatically reduced the tumor number and tumor size in both distal/mid-colon followed by reduction in disease-activity index. Crocin also suppressed the colonic inflammation induced by dextran-sulfate-sodium and notably recovered the increased levels of MDA, decreased thiol levels and activity of CAT levels. Crocin was able to ameliorate the severe inflammation with mucosal ulcers and high-grade dysplastic crypts as detected by inflammation score, crypt loss, pathological changes and histology scores. We demonstrated an antitumor activity of crocin in CRC and its potential role in improvement of inflammation with mucosal ulcers and high-grade dysplastic crypts, supporting the desireability of further investigations on the therapeutic potential of this approach in CRC.

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Section: Discussionmentioning

confidence: 99%

Crocin synergistically enhances the antiproliferative activity of 5‐flurouracil through Wnt/PI3K pathway in a mouse model of colitis‐associated colorectal cancer

Amerizadeh

Rezaei

Rahmani

et al. 2018

J of Cellular Biochemistry

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“…The treatment could not affect the levels of TNF- α , SIRT1, and LC3 when NF- κ B was silenced, suggesting that picroside II treatment may affect the levels of TNF- α , SIRT1, and LC3 via NF- κ B. The overexpression of TNF- α is significantly correlated with the expression of NF- κ B [22], suggesting that the expression of TNF- α may increase the expression of NF- κ B or the expression of NF- κ B may improve the expression of TNF- α . To determine which one was determinant, NF- κ B was silenced and the results demonstrated NF- κ B silence resulted in the decrease of TNF- α level (Figure 8(c)).…”

Section: Discussionmentioning

confidence: 99%

“…Blocking the activation of NF- κ B appears to reduce the inflammatory response in SAP [21]. TNF- α is a multifunctional proinflammatory cytokine and is significantly correlated with the expression of NF- κ B [22]. On the other hand, overexpression of NF- κ B promotes the expression of TNF-alpha-induced-SIRT1.…”

Section: Introductionmentioning

confidence: 99%

Picroside II Shows Protective Functions for Severe Acute Pancreatitis in Rats by Preventing NF‐κB‐Dependent Autophagy

Piao¹,

Liu

Guo

et al. 2017

Oxidative Medicine and Cellular Longevity

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Picroside II, from the herb Picrorhiza scrophulariiflora Pennell, has antioxidant and anti-inflammatory activities. However, its function on severe acute pancreatitis (SAP) and molecular mechanism remains unknown. The effects of picroside II on the SAP induced by cerulean were investigated. SAP rats were treated with picroside II (25 mg/kg). The severity of SAP was evaluated by using biochemical and histological analyses. Pancreatic cancer cell PANC-1 was transfected with ptfLC3 (an indicator of autophagic activity), pcDNA3.1-NF-κB (nuclear factor kappa B), and pTZU6+1-NF-κB-shRNA and then treated with picroside II. Relative molecules related with NF-κB-dependent autophagy were detected by using Western blot. Autophagic activities were observed by phase-contrast and fluorescent microscopes. Acetylated LC3 was detected by immunoprecipitation. The results showed that picroside II treatment reduced the level of ALT, AST, NF-κB, IL-1β, IL-6, TNF-α, and SIRT1 (NAD+-dependent deacetylase) and increased the level of SOD and GSH. The autophagic activity was reduced when NF-κB was silenced, and the levels of TNF-α and SIRT1 were reduced. In contrast, the overexpression of NF-κB increased autophagic activity and the level of TNF-α, which activated SIRT1. SIRT1 deacetylated LC3 and increased autophagic activities. Picroside II ameliorates SAP by improving antioxidant and anti-inflammtory activities of SAP models via NF-κB-dependent autophagy.

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“…Inflammation is one of the hallmarks of colorectal cancer contributing to malignant transformation and tumor progression [71,72]. Activation of pro-inflammatory NF-κB signaling pathway inducing increased iNOS expression is one of the mechanisms of colorectal cancer development [38,73]. Besides that, the participation of eNOS isoform in colorectal cancer carcinogenesis has been shown by other authors [38,39,[73][74][75].…”

Section: Cell Growthmentioning

confidence: 91%

“…Although increased expression of the three NOS isoforms in different cancers has been related in innumerous studies, not all the studies describe NOS activity [13,[38][39][40][41]. High NOS expression is associated with increased cell proliferation, metastasis, and chemotherapy resistance, in some cases being associated with poor prognosis [26,40,42].…”

Section: Nitric Oxide Synthasementioning

confidence: 99%

The Role of the BH4 Cofactor in Nitric Oxide Synthase Activity and Cancer Progression: Two Sides of the Same Coin

Gonçalves

Jasiulionis

Melo

2021

IJMS

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Cancer development is associated with abnormal proliferation, genetic instability, cell death resistance, metabolic reprogramming, immunity evasion, and metastasis. These alterations are triggered by genetic and epigenetic alterations in genes that control cell homeostasis. Increased reactive oxygen and nitrogen species (ROS, RNS) induced by different enzymes and reactions with distinct molecules contribute to malignant transformation and tumor progression by modifying DNA, proteins, and lipids, altering their activities. Nitric oxide synthase plays a central role in oncogenic signaling modulation and redox landscape. Overexpression of the three NOS isoforms has been found in innumerous types of cancer contributing to tumor growth and development. Although the main function of NOS is the production of nitric oxide (NO), it can be a source of ROS in some pathological conditions. Decreased tetrahydrobiopterin (BH4) cofactor availability is involved in NOS dysfunction, leading to ROS production and reduced levels of NO. The regulation of NOSs by BH4 in cancer is controversial since BH4 has been reported as a pro-tumoral or an antitumoral molecule. Therefore, in this review, the role of BH4 in the control of NOS activity and its involvement in the capabilities acquired along tumor progression of different cancers was described.

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Oral Concentrated Grape Juice Suppresses Expression of NF-kappa B, TNF-α and iNOS in Experimentally Induced Colorectal Carcinogenesis in Wistar Rats

Cited by 10 publications

References 29 publications

Crocin synergistically enhances the antiproliferative activity of 5‐flurouracil through Wnt/PI3K pathway in a mouse model of colitis‐associated colorectal cancer

Crocin synergistically enhances the antiproliferative activity of 5‐flurouracil through Wnt/PI3K pathway in a mouse model of colitis‐associated colorectal cancer

Picroside II Shows Protective Functions for Severe Acute Pancreatitis in Rats by Preventing NF‐κB‐Dependent Autophagy

The Role of the BH4 Cofactor in Nitric Oxide Synthase Activity and Cancer Progression: Two Sides of the Same Coin

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