Modulatory effect of betanin on high glucose induced epithelial to mesenchymal transition in renal proximal tubular cells

Sutariya, Brijesh; Taneja, Neetika; Badgujar, Lohit; Saraf, M. N.

doi:10.1016/j.biopha.2017.02.006

Cited by 7 publications

(3 citation statements)

References 30 publications

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“…The dose–response relationship between fruit and vegetable consumption, cardiovascular risk, and cancer mortality was quantified in a recent meta-analysis, providing further evidence that the higher consumption of fruit and vegetables, and consequently antioxidants, is associated with a lower risk of all-cause mortality, mainly cancer and cardiovascular diseases [23]. In addition, previous chronic human studies using high amounts of beetroot and, consequently, high doses of betanin, NO 3 − , phenolic compounds, and organic acids, through juice, gel, and cereal bar intake provided biochemical benefits and vascular effects without adverse outcomes [63,64,65]. Furthermore, to reach the beneficial biochemical effects, betanin, for the intake of other bioactive compounds, requires a supplementation period to reduce oxidative stress parameters [35,36].…”

Section: Discussionmentioning

confidence: 97%

Short-Term Betanin Intake Reduces Oxidative Stress in Wistar Rats

et al. 2019

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Oxidative stress is a common condition described in risk factors for cardiovascular disease. Betanin, a bioactive pigment from red beetroot demonstrates anti-inflammatory and antioxidant properties. The main aim of this study was to evaluate the short-term intake of betanin against oxidative stress in a rodent model, a common condition described in several risk factors for cardiovascular disease. Oxidative stress was induced in Wistar rats by a hyperlipidemic diet for 60 days, followed by betanin administration (20 mg·kg−1) through oral gavage for 20 days. Plasma biochemical parameters and antioxidant enzyme activities were evaluated. Lipid peroxidation and histopathological changes were determined in the liver. The hyperlipidemic diet caused hyperglycemia, hyperinsulinemia, insulin resistance, and increases in alanine transaminase and aspartate transaminase levels. Oxidative stress status was confirmed by reduction of antioxidant enzyme activities, increased lipid peroxidation, and liver damage. Purified betanin regulated glucose levels, insulin, and insulin resistance. Hepatic damage was reversed as evidenced by the reduction in alanine transaminase and aspartate transaminase levels and confirmed by histological analyses. Betanin reduced hepatic malondialdehyde and increased superoxide dismutase, catalase, and glutathione peroxidase activities. Short-term betanin intake modulated biochemical parameters, reversed hepatic tissue damage, and attenuated oxidative stress in Wistar rats.

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Section: Discussionmentioning

confidence: 97%

Short-Term Betanin Intake Reduces Oxidative Stress in Wistar Rats

et al. 2019

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“…This is in agreement with a previous study that reported the efficacy of BET in the treatment of renal fibrosis by regulating the EMT process in NRK-52E cells. 51 These results indicated that BET regulates EMT by suppressing oxidative stress, TGF-β1, and regulating NLRP3.…”

Section: Discussionmentioning

confidence: 81%

Betanin protects against bleomycin-induced pulmonary fibrosis by regulating the NLRP3/IL-1β/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition

Abd Elrazik,

Helmy

2024

Food Funct.

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“…Betanin from beets can decrease the production of superoxide anion and cytokines TNF-α and IL-1 [113,114]. Betanin (25-50 µM) can inhibit high glucose-induced EMT of renal proximal tubular cells [115]. However, activity of betanin for EMT of cancer cells has not been reported yet.…”

Section: Reversal Of Emt By Anti-inflammatory Natural Compoundsmentioning

confidence: 99%

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Lee

2019

Cancers

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Epithelial mesenchymal transition (EMT) is a key process in the progression of malignant cancer. Therefore, blocking the EMT can be a critical fast track for the development of anticancer drugs. In this paper, we update recent research output of EMT and we explore suppression of EMT by natural anti-inflammatory compounds and pro-resolving lipids.A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the m ajor signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2) belongs to the runt-related transcription factor family [19]. Runx2 plays a key role in EMT of hepatocellular carcinoma (HCC) [20]. GATA transcription factors are also implicated in the EMT of cancer cells [21].A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the major signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2...

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Modulatory effect of betanin on high glucose induced epithelial to mesenchymal transition in renal proximal tubular cells

Cited by 7 publications

References 30 publications

Short-Term Betanin Intake Reduces Oxidative Stress in Wistar Rats

Short-Term Betanin Intake Reduces Oxidative Stress in Wistar Rats

Betanin protects against bleomycin-induced pulmonary fibrosis by regulating the NLRP3/IL-1β/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

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