Be consistent: Consistency is key when taking any dietary supplement. It is generally recommended to take luteolin supplements regularly as part of a daily routine for maximum benefits. If you have any concerns or questions about the duration of use, consult your healthcare provider. Luteolin is potent to activate both the extrinsic and intrinsic apoptosis pathways. Direct increase in expression of the death receptor 5 (DR5), the functional receptor for TRAIL, has been demonstrated in cervical and prostate cancer cells, which is accompanied by activation of caspase-8, −10, −9 and −3, and cleavage of Bcl-2-interacting domain (BID). The increase of DR5 expression is likely through activated transcription of the dr5 gene [ 105]. Interestingly, DR5 was not induced and no cytotoxicity was observed in luteolin-treated normal human peripheral blood mononuclear cells [ 105]. Luteolin was also found to enhance expression of Fas to induce apoptosis in human hepatoma cells through triggering the degradation of STAT3, a known negative regulator of fas transcription [ 106].

Luteolin, like most other flavonoids, has antioxidant properties. The Reactive Oxygen Species or ROS are a large group of reactive species with Oxygen and a short life span. When produced in large amounts, these species are often responsible for severe conditions like damage to protein, lipids, and even DNA. Park SH, Ham S, Kwon TH, Kim MS, Lee DH, Kang JW, Oh SR, Yoon DY. Luteolin induces cell cycle arrest and apoptosis through extrinsic and intrinsic signaling pathways in MCF-7 breast cancer cells. J Environ Pathol Toxicol Oncol. 2014;33(3):219–31.As a powerful bioflavonoid, Luteolin boasts antioxidant properties that support brain health, function, and cognition. A cell line study suggests that luteolin (and quercetin) “display progesterone antagonist activity beneficial in a breast cancer model but deleterious in an endometrial cancer model.” However, this is just a cell line study, and it only suggests caution with consuming luteolin via supplement, not from a plant-rich diet. The flavonoid also sometimes chelates the transition metal ions that are the primary reason behind the production of ROS. Luteolin is a type of flavonoid, which is a class of compounds that are found in a wide variety of fruits and vegetables.

Potočnjak I, Šimić L, Gobin I, Vukelić I, Domitrović R. Antitumor activity of luteolin in human colon cancer SW620 cells is mediated by the ERK/FOXO3a signaling pathway. Toxicol In Vitro. 2020;66:104852. Its ability to scavenge ROS using its mechanism. The double bond present between carbon 2 and 3 and the carbonyl group is responsible for the scavenging process. Sun DW, Zhang HD, Mao L, Mao CF, Chen W, Cui M, Ma R, Cao HX, Jing CW, Wang Z, et al. Luteolin inhibits breast Cancer Development and Progression in Vitro and in vivo by suppressing Notch Signaling and regulating MiRNAs. Cell Physiol Biochem. 2015;37(5):1693–711.Ashrafizadeh M, Ahmadi Z, Farkhondeh T, Samarghandian S. Autophagy regulation using luteolin: new insight into its anti-tumor activity. Cancer Cell Int. 2020;20(1):537. Estrogens are hormones involved in the proliferation and differentiation of their target cells. In response to estrogens, the estrogen receptor (ER) is activated to stimulate DNA synthesis and cell proliferation [ 36]. Flavonoids are naturally occurring phytoestrogens because they can bind to ERs and activate their signaling pathways [ 37- 39]. Because luteolin possesses potent estrogenic activity at low concentrations, it could be a useful agent for hormone replacement therapy [ 40]. aSquared Nutrition’s dedication to quality shines through as this Luteolin supplement is crafted with all-natural ingredients, is non-GMO, vegan-friendly, and gluten-free, catering to diverse dietary preferences and needs. Naiki-Ito A, Naiki T, Kato H, Iida K, Etani T, Nagayasu Y, Suzuki S, Yamashita Y, Inaguma S, Onishi M, et al. Recruitment of miR-8080 by luteolin inhibits androgen receptor splice variant 7 expression in castration-resistant prostate cancer. Carcinogenesis. 2019;41(8):1145–57.