Hesperetin Inhibits Vascular Formation by Suppressing of the PI3K/AKT, ERK, and p38 MAPK Signaling Pathways
Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti...
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| Published in | Preventive nutrition and food science Vol. 19; no. 4; pp. 299 - 306 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
Korea (South)
한국식품영양과학회
01.12.2014
The Korean Society of Food Science and Nutrition |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2287-1098 2287-8602 |
| DOI | 10.3746/pnf.2014.19.4.299 |
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| Abstract | Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of hesperetin (25, 50, and 100 μM) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling. |
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| AbstractList | Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of hesperetin (25, 50, and 100 μM) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling. Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of hesperetin (25, 50, and 100 μM) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs ( P <0.05). Moreover, hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling. Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of hesperetin (25, 50, and 100 M) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling. KCI Citation Count: 1 Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of hesperetin (25, 50, and 100 μM) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling.Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of hesperetin (25, 50, and 100 μM) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling. |
| Author | Gi Dae Kim |
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| Cites_doi | 10.1038/nrc1628 10.1016/S0955-2863(02)00204-8 10.1038/sj.onc.1206921 10.1016/j.nut.2006.05.004 10.1021/np040031y 10.1093/jnci/82.1.4 10.1161/01.RES.0000022200.71892.9F 10.1002/ptr.1074 10.1124/mol.105.020537 10.1373/49.1.32 10.1007/s00432-002-0373-y 10.1016/S0092-8674(00)81683-9 10.1006/bbrc.1999.2018 10.1038/nature04483 10.1016/j.canlet.2004.07.013 10.1158/0008-5472.CAN-07-5944 10.1016/j.coph.2008.08.004 10.3892/ijo.2013.1959 10.1016/S0165-6147(00)01676-X 10.1007/978-1-4419-8871-3_1 10.1136/jcp.2004.025536 10.1128/AEM.58.8.2375-2380.1992 10.2133/dmpk.19.245 10.1038/nprot.2011.435 10.1038/nature10144 10.1016/j.cardiores.2005.09.019 10.1074/jbc.M302967200 10.1016/j.toxlet.2008.05.023 10.1159/000341455 10.4161/cbt.7.12.6967 10.1161/CIRCRESAHA.107.167171 10.1002/mnfr.201100680 10.1038/sj.onc.1203533 10.1096/fj.01-0300rev |
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| Keywords | vascular formation hesperetin HUVECs PI3K/AKT |
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| References | (E1FSA3_2014_v19n4_299_023) 2012; 30 (E1FSA3_2014_v19n4_299_005) 2005; 438 (E1FSA3_2014_v19n4_299_022) 2004; 67 (E1FSA3_2014_v19n4_299_025) 1997; 57 (E1FSA3_2014_v19n4_299_014) 1992; 58 (E1FSA3_2014_v19n4_299_010) 2006; 69 (E1FSA3_2014_v19n4_299_032) 2000; 100 (E1FSA3_2014_v19n4_299_017) 2006; 22 (E1FSA3_2014_v19n4_299_031) 2006; 69 (E1FSA3_2014_v19n4_299_003) 2008; 102 (E1FSA3_2014_v19n4_299_011) 2008; 8 (E1FSA3_2014_v19n4_299_034) 2002; 128 (E1FSA3_2014_v19n4_299_021) 2005; 5 (E1FSA3_2014_v19n4_299_007) 2000; 19 (E1FSA3_2014_v19n4_299_033) 2008; 7 (E1FSA3_2014_v19n4_299_008) 2004; 23 (E1FSA3_2014_v19n4_299_019) 2008; 68 (E1FSA3_2014_v19n4_299_027) 2002; 16 (E1FSA3_2014_v19n4_299_029) 2003; 49 (E1FSA3_2014_v19n4_299_028) 2004; 215 (E1FSA3_2014_v19n4_299_004) 1990; 82 (E1FSA3_2014_v19n4_299_001) 2004; 117 (E1FSA3_2014_v19n4_299_012) 2001; 15 (E1FSA3_2014_v19n4_299_030) 2000; 268 (E1FSA3_2014_v19n4_299_002) 2011; 473 (E1FSA3_2014_v19n4_299_015) 2004; 19 (E1FSA3_2014_v19n4_299_009) 2003; 278 (E1FSA3_2014_v19n4_299_006) 2005; 58 (E1FSA3_2014_v19n4_299_024) 2013; 43 (E1FSA3_2014_v19n4_299_036) 2002; 90 (E1FSA3_2014_v19n4_299_035) 2001; 22 (E1FSA3_2014_v19n4_299_018) 2008; 180 (E1FSA3_2014_v19n4_299_016) 2012; 56 (E1FSA3_2014_v19n4_299_013) 2002; 128 (E1FSA3_2014_v19n4_299_026) 2002; 13 (E1FSA3_2014_v19n4_299_020) 2011; 7 11746857 - Phytother Res. 2001 Dec;15(8):655-69 16424078 - Mol Pharmacol. 2006 Apr;69(4):1226-33 12384797 - J Cancer Res Clin Oncol. 2002 Oct;128(10):539-46 10815805 - Oncogene. 2000 Apr 20;19(17 ):2138-46 9230201 - Cancer Res. 1997 Jul 15;57(14):2916-21 12089061 - Circ Res. 2002 Jun 28;90(12):1243-50 16815676 - Nutrition. 2006 Sep;22(9):947-51 18721898 - Curr Opin Pharmacol. 2008 Aug;8(4):393-412 14712224 - Oncogene. 2004 Jan 8;23(1):192-200 10647931 - Cell. 2000 Jan 7;100(1):57-70 11772931 - FASEB J. 2002 Jan;16(1):2-14 15332835 - J Nat Prod. 2004 Aug;67(8):1216-38 12816951 - J Biol Chem. 2003 Sep 12;278(37):35501-7 12121824 - J Nutr Biochem. 2002 Jul;13(7):380-390 15488631 - Cancer Lett. 2004 Nov 25;215(2):129-40 16355214 - Nature. 2005 Dec 15;438(7070):967-74 16254106 - J Clin Pathol. 2005 Nov;58(11):1170-4 10652234 - Biochem Biophys Res Commun. 2000 Feb 5;268(1):183-91 23708970 - Int J Oncol. 2013 Aug;43(2):600-10 18981713 - Cancer Biol Ther. 2008 Dec;7(12):1994-2003 1514785 - Appl Environ Microbiol. 1992 Aug;58(8):2375-80 15499193 - Drug Metab Pharmacokinet. 2004 Aug;19(4):245-63 18339865 - Cancer Res. 2008 Mar 15;68(6):1843-50 18369162 - Circ Res. 2008 Mar 28;102(6):637-52 21593862 - Nature. 2011 May 19;473(7347):298-307 22890153 - Cell Physiol Biochem. 2012;30(3):758-70 22707269 - Mol Nutr Food Res. 2012 Jun;56(6):945-56 22193302 - Nat Protoc. 2011 Dec 22;7(1):89-104 18590808 - Toxicol Lett. 2008 Aug 28;180(3):166-73 1688381 - J Natl Cancer Inst. 1990 Jan 3;82(1):4-6 12507958 - Clin Chem. 2003 Jan;49(1):32-40 15928673 - Nat Rev Cancer. 2005 Jun;5(6):423-35 15015550 - Cancer Treat Res. 2004;117:3-32 16336951 - Cardiovasc Res. 2006 Feb 1;69(2):512-9 11282421 - Trends Pharmacol Sci. 2001 Apr;22(4):201-7 |
| References_xml | – volume: 5 start-page: 423 year: 2005 ident: E1FSA3_2014_v19n4_299_021 publication-title: Nat Rev Cancer doi: 10.1038/nrc1628 – volume: 13 start-page: 380 year: 2002 ident: E1FSA3_2014_v19n4_299_026 publication-title: J Nutr Biochem doi: 10.1016/S0955-2863(02)00204-8 – volume: 23 start-page: 192 year: 2004 ident: E1FSA3_2014_v19n4_299_008 publication-title: Oncogene doi: 10.1038/sj.onc.1206921 – volume: 22 start-page: 947 year: 2006 ident: E1FSA3_2014_v19n4_299_017 publication-title: Nutrition doi: 10.1016/j.nut.2006.05.004 – volume: 67 start-page: 1216 year: 2004 ident: E1FSA3_2014_v19n4_299_022 publication-title: J Nat Prod doi: 10.1021/np040031y – volume: 82 start-page: 4 year: 1990 ident: E1FSA3_2014_v19n4_299_004 publication-title: J Natl Cancer Inst doi: 10.1093/jnci/82.1.4 – volume: 90 start-page: 1243 year: 2002 ident: E1FSA3_2014_v19n4_299_036 publication-title: Circ Res doi: 10.1161/01.RES.0000022200.71892.9F – volume: 15 start-page: 655 year: 2001 ident: E1FSA3_2014_v19n4_299_012 publication-title: Phytother Res doi: 10.1002/ptr.1074 – volume: 69 start-page: 1226 year: 2006 ident: E1FSA3_2014_v19n4_299_031 publication-title: Mol Pharmacol doi: 10.1124/mol.105.020537 – volume: 49 start-page: 32 year: 2003 ident: E1FSA3_2014_v19n4_299_029 publication-title: Clin Chem doi: 10.1373/49.1.32 – volume: 128 start-page: 539 year: 2002 ident: E1FSA3_2014_v19n4_299_013 publication-title: J Cancer Res Clin Oncol doi: 10.1007/s00432-002-0373-y – volume: 100 start-page: 57 year: 2000 ident: E1FSA3_2014_v19n4_299_032 publication-title: Cell doi: 10.1016/S0092-8674(00)81683-9 – volume: 268 start-page: 183 year: 2000 ident: E1FSA3_2014_v19n4_299_030 publication-title: Biochem Biophys Res Commun doi: 10.1006/bbrc.1999.2018 – volume: 438 start-page: 967 year: 2005 ident: E1FSA3_2014_v19n4_299_005 publication-title: Nature doi: 10.1038/nature04483 – volume: 215 start-page: 129 year: 2004 ident: E1FSA3_2014_v19n4_299_028 publication-title: Cancer Lett doi: 10.1016/j.canlet.2004.07.013 – volume: 68 start-page: 1843 year: 2008 ident: E1FSA3_2014_v19n4_299_019 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-07-5944 – volume: 8 start-page: 393 year: 2008 ident: E1FSA3_2014_v19n4_299_011 publication-title: Curr Opin Pharmacol doi: 10.1016/j.coph.2008.08.004 – volume: 43 start-page: 600 year: 2013 ident: E1FSA3_2014_v19n4_299_024 publication-title: Int J Oncol doi: 10.3892/ijo.2013.1959 – volume: 22 start-page: 201 year: 2001 ident: E1FSA3_2014_v19n4_299_035 publication-title: Trends Pharmacol Sci doi: 10.1016/S0165-6147(00)01676-X – volume: 117 start-page: 3 year: 2004 ident: E1FSA3_2014_v19n4_299_001 publication-title: Cancer Treat Res doi: 10.1007/978-1-4419-8871-3_1 – volume: 58 start-page: 1170 year: 2005 ident: E1FSA3_2014_v19n4_299_006 publication-title: J Clin Pathol doi: 10.1136/jcp.2004.025536 – volume: 58 start-page: 2375 year: 1992 ident: E1FSA3_2014_v19n4_299_014 publication-title: Appl Environ Microbiol doi: 10.1128/AEM.58.8.2375-2380.1992 – volume: 19 start-page: 245 year: 2004 ident: E1FSA3_2014_v19n4_299_015 publication-title: Drug Metab Pharmacokinet doi: 10.2133/dmpk.19.245 – volume: 7 start-page: 89 year: 2011 ident: E1FSA3_2014_v19n4_299_020 publication-title: Nat Protoc doi: 10.1038/nprot.2011.435 – volume: 473 start-page: 298 year: 2011 ident: E1FSA3_2014_v19n4_299_002 publication-title: Nature doi: 10.1038/nature10144 – volume: 69 start-page: 512 year: 2006 ident: E1FSA3_2014_v19n4_299_010 publication-title: Cardiovasc Res doi: 10.1016/j.cardiores.2005.09.019 – volume: 57 start-page: 2916 year: 1997 ident: E1FSA3_2014_v19n4_299_025 publication-title: Cancer Res – volume: 278 start-page: 35501 year: 2003 ident: E1FSA3_2014_v19n4_299_009 publication-title: J Biol Chem doi: 10.1074/jbc.M302967200 – volume: 180 start-page: 166 year: 2008 ident: E1FSA3_2014_v19n4_299_018 publication-title: Toxicol Lett doi: 10.1016/j.toxlet.2008.05.023 – volume: 30 start-page: 758 year: 2012 ident: E1FSA3_2014_v19n4_299_023 publication-title: Cell Physiol Biochem doi: 10.1159/000341455 – volume: 7 start-page: 1994 year: 2008 ident: E1FSA3_2014_v19n4_299_033 publication-title: Cancer Biol Ther doi: 10.4161/cbt.7.12.6967 – volume: 102 start-page: 637 year: 2008 ident: E1FSA3_2014_v19n4_299_003 publication-title: Circ Res doi: 10.1161/CIRCRESAHA.107.167171 – volume: 56 start-page: 945 year: 2012 ident: E1FSA3_2014_v19n4_299_016 publication-title: Mol Nutr Food Res doi: 10.1002/mnfr.201100680 – volume: 19 start-page: 2138 year: 2000 ident: E1FSA3_2014_v19n4_299_007 publication-title: Oncogene doi: 10.1038/sj.onc.1203533 – volume: 16 start-page: 2 year: 2002 ident: E1FSA3_2014_v19n4_299_027 publication-title: FASEB J doi: 10.1096/fj.01-0300rev – volume: 128 start-page: 539 year: 2002 ident: E1FSA3_2014_v19n4_299_034 publication-title: J Cancer Res Clin Oncol doi: 10.1007/s00432-002-0373-y – reference: 12507958 - Clin Chem. 2003 Jan;49(1):32-40 – reference: 21593862 - Nature. 2011 May 19;473(7347):298-307 – reference: 10647931 - Cell. 2000 Jan 7;100(1):57-70 – reference: 11772931 - FASEB J. 2002 Jan;16(1):2-14 – reference: 18590808 - Toxicol Lett. 2008 Aug 28;180(3):166-73 – reference: 22890153 - Cell Physiol Biochem. 2012;30(3):758-70 – reference: 12816951 - J Biol Chem. 2003 Sep 12;278(37):35501-7 – reference: 15015550 - Cancer Treat Res. 2004;117:3-32 – reference: 12384797 - J Cancer Res Clin Oncol. 2002 Oct;128(10):539-46 – reference: 16254106 - J Clin Pathol. 2005 Nov;58(11):1170-4 – reference: 12121824 - J Nutr Biochem. 2002 Jul;13(7):380-390 – reference: 15499193 - Drug Metab Pharmacokinet. 2004 Aug;19(4):245-63 – reference: 1688381 - J Natl Cancer Inst. 1990 Jan 3;82(1):4-6 – reference: 9230201 - Cancer Res. 1997 Jul 15;57(14):2916-21 – reference: 18721898 - Curr Opin Pharmacol. 2008 Aug;8(4):393-412 – reference: 16815676 - Nutrition. 2006 Sep;22(9):947-51 – reference: 16336951 - Cardiovasc Res. 2006 Feb 1;69(2):512-9 – reference: 15928673 - Nat Rev Cancer. 2005 Jun;5(6):423-35 – reference: 23708970 - Int J Oncol. 2013 Aug;43(2):600-10 – reference: 16355214 - Nature. 2005 Dec 15;438(7070):967-74 – reference: 18981713 - Cancer Biol Ther. 2008 Dec;7(12):1994-2003 – reference: 15332835 - J Nat Prod. 2004 Aug;67(8):1216-38 – reference: 18339865 - Cancer Res. 2008 Mar 15;68(6):1843-50 – reference: 11746857 - Phytother Res. 2001 Dec;15(8):655-69 – reference: 11282421 - Trends Pharmacol Sci. 2001 Apr;22(4):201-7 – reference: 12089061 - Circ Res. 2002 Jun 28;90(12):1243-50 – reference: 10815805 - Oncogene. 2000 Apr 20;19(17 ):2138-46 – reference: 22193302 - Nat Protoc. 2011 Dec 22;7(1):89-104 – reference: 15488631 - Cancer Lett. 2004 Nov 25;215(2):129-40 – reference: 18369162 - Circ Res. 2008 Mar 28;102(6):637-52 – reference: 16424078 - Mol Pharmacol. 2006 Apr;69(4):1226-33 – reference: 1514785 - Appl Environ Microbiol. 1992 Aug;58(8):2375-80 – reference: 14712224 - Oncogene. 2004 Jan 8;23(1):192-200 – reference: 10652234 - Biochem Biophys Res Commun. 2000 Feb 5;268(1):183-91 – reference: 22707269 - Mol Nutr Food Res. 2012 Jun;56(6):945-56 |
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| Title | Hesperetin Inhibits Vascular Formation by Suppressing of the PI3K/AKT, ERK, and p38 MAPK Signaling Pathways |
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