Abstract
Apigenin (AP) is a plant flavonoid with potential biomedical applications. To enhance the anti-tumour effect, AP was deuterated via hydrogen–deuterium exchange under hydrothermal conditions. The anti-tumor effects of deuterated AP (D-AP) were then tested on HCT116 cells and on a murine model of turpentine-induced inflammation. Cell cycle progression and cell proliferation were measured by flow cytometry, and in vivo immuno-inflammation was evaluated by quantitating glucose metabolism using 18F-fluorodeoxyglucose positron emission tomography. According to the mass spectral results, the efficiency of AP deuteration was 62.96%. For both the two groups of AP and D-AP at 24 h and 48 h, there were an obvious increase on perception of G2 phage. Apigenin showed the ability of blocking in G2 phage to inhibit cellular proliferation. Additionally, D-AP induced early apoptosis in more cells than did AP (12.1% vs. 10.4%). Moreover, D-AP induced a more severe process of anti-inflammation during the early period, resulting in a more effective anti-inflammatory response. Therefore, given the innate ability of D-AP to block cell proliferation and induce early apoptosis, we conclude that deuteration enhances the systemic anti-cancer effect of this flavonoid.
Highlights
Many specific and efficient flavonoid compounds have been explored and applied in food and drug development owing to their high bioactivities [1, 2, 3]
This study focused on the systemic anti-tumour effect of deuterated AP (D-AP), including its influence on tumour cell proliferation, apoptosis induction, and immuno-inflammatory responses
51.69%, 58.85%, and 62.96% of the hydrogen atoms of AP were deuterated after the first (DAP1), second (D-AP2), and third (D-AP3) hydrogen–deuterium exchange (HDX) reactions, respectively
Summary
Many specific and efficient flavonoid compounds have been explored and applied in food and drug development owing to their high bioactivities [1, 2, 3]. AP acts in two ways [5, 6]. It controls tumour cell proliferation (including apoptosis or autophagy induction), cell cycle regulation, and migration or invasion inhibition. It inhibits the proliferation of pancreatic cancer cells by arresting the G2/M phase of the cell cycle [7]. The flavonoid indirectly affects tumour progression by stimulating the systemic immune response, such as by inhibiting the expression of nitrix oxide synthase, cyclooxygenase, and pro-inflammatory cytokines [8, 9]
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