2011
DOI: 10.1016/j.cbi.2010.09.028
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Naringenin, a flavanone inhibits the proliferation of cerebrally implanted C6 glioma cells in rats

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Cited by 43 publications
(35 citation statements)
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“…In addition, naringenin is known to suppress various NF‐κB‐regulated gene products including vascular endothelial growth factor (VEGF), the proinflammatory enzyme cyclooxigenase 2 (COX2), matrix metalloproteinase‐2 and matrix metalloproteinase‐9 (MMP‐2 and MMP‐9), which are associated with tumour progression and metastasis. Several studies on human cancer and animal tumour model have documented that increased tumour expression of COX‐2, VEGF, MMP‐2 and MMP‐9 was correlated with more aggressive lesions that sustain inflammation, tumour growth, progression and metastasis. Consistent with earlier findings, angiogenic effects of VEGF seen in the present study are also mediated via the upregulation of MMPs that degrade the components of the extracellular matrix (ECM) during metastatic dissemination of tumour cells promote tumour invasion and metastasis .…”
Section: Discussionmentioning
confidence: 99%
“…In addition, naringenin is known to suppress various NF‐κB‐regulated gene products including vascular endothelial growth factor (VEGF), the proinflammatory enzyme cyclooxigenase 2 (COX2), matrix metalloproteinase‐2 and matrix metalloproteinase‐9 (MMP‐2 and MMP‐9), which are associated with tumour progression and metastasis. Several studies on human cancer and animal tumour model have documented that increased tumour expression of COX‐2, VEGF, MMP‐2 and MMP‐9 was correlated with more aggressive lesions that sustain inflammation, tumour growth, progression and metastasis. Consistent with earlier findings, angiogenic effects of VEGF seen in the present study are also mediated via the upregulation of MMPs that degrade the components of the extracellular matrix (ECM) during metastatic dissemination of tumour cells promote tumour invasion and metastasis .…”
Section: Discussionmentioning
confidence: 99%
“…Naringenin triggered the C6 glioma cells cerebrally implanted in rat to undergo apoptosis by upregulating connexin 43, reducing the Bcl‐2/Bax ratio, and increasing the activities of caspase‐3 and ‐9 . Administering naringenin also attenuated the expression of protein kinase C, cyclin D1, and cyclin‐dependent protein kinase 4, which in turn suppressed the proliferation of cerebrally implanted C6 glioma cells in rats . Stompor et al reported that treatment with naringenin at 150, 250, and 500 μM for 24 hours reduced the cell viability to 60%, 50%, and below 20%, respectively, in GBM U‐118 MG cells.…”
Section: Discussionmentioning
confidence: 99%
“…The scheme of naringenin administration is due to its increasing availability in plasma immediately after it is ingested (Wang et al, 2014b; Mata‐Bilbao Mde et al, 2007). The dose was defined according to its neuroprotective action reported in the literature (Raza et al, 2013; Sabarinathan et al, 2011).…”
Section: Methodsmentioning
confidence: 99%