Malaysian Tualang honey suppresses the angiogenic events in endothelial cells induced by vascular endothelial growth factor

Anti-VEGF therapy has been used as the anti-angiogenic agent in cancer treatment. However, the treatment often couples with severe complications. Complementary natural products that offer similar anti-angiogenic potency with less side effects are sought as alternatives. Study showed that Malaysian T...

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Main Authors: Ahmad Firdaus Abdul Khalid,, Ng, Chin Theng, Fong, Lai Yen, Tan, Jun Jie, Fahmi Yakop,, Nur Aqilah Kamaruddin,, Muhammad Nazrul Hakim Abdullah,, Yong, Yoke Keong
Format: Article
Language:English
Published: Penerbit Universiti Kebangsaan Malaysia 2022
Online Access:http://journalarticle.ukm.my/19166/1/15.pdf
http://journalarticle.ukm.my/19166/
https://www.ukm.my/jsm/malay_journals/jilid51bil3_2022/KandunganJilid51Bil3_2022.html
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Summary:Anti-VEGF therapy has been used as the anti-angiogenic agent in cancer treatment. However, the treatment often couples with severe complications. Complementary natural products that offer similar anti-angiogenic potency with less side effects are sought as alternatives. Study showed that Malaysian Tualang Honey (MTH) can inhibit inflammation-induced vascular hyperpermeability in vitro and in vivo, but the effect on the angiogenesis process remains unclear. Thus, this study aims to determine the anti-angiogenic effects of MTH. Effects of MTH ranging from 0.3% to 0.9% on VEGF-induced human umbilical vein endothelial cells (HUVEC) angiogenesis was determined by proliferation, migration and tube-formation assays. Matrix metalloproteinase-2 (MMP-2) secretion from HUVEC and VEGF production from MCF7 cancer cells in response to MTH were also quantified by using ELISA kits. Suramin, an angio-suppressive agent was used as positive control. MTH significantly suppressed HUVEC proliferation (from 155% proliferation rate to 54%); migration (~ 50% inhibition rate) and tube-formation (69% reduction) induced by VEGF. These findings were explained by the significant reduction (p < 0.05) of VEGF-induced MMP-2 secretion in HUVEC with 39% suppression exhibited by 0.9% of MTH. MTH also significantly (p < 0.05) reduced VEGF secretion (19% reduction compared to control) in MCF7 breast cancer cells. Our findings suggest that the anti-angiogenic effects of MTH mainly targets endothelial cell through inhibition cell proliferation, migration and tube formation capacity, via suppression of MMP-2 secretion by the endothelial cells. However, MTH has less prominent effect on suppressing VEGF secretion by the MCF7 cancer cells.