The combined effect of pomegranate extract and tangeretin on the DMBA-induced breast cancer model

N‐(benzylidene)‐2‐((2‐hydroxynaphthalen‐1‐yl)diazenyl)benzohydrazides (1‐2) (NCHDH and NTHDH) attenuate DMBA‐induced breast cancer via Nrf2/NF‐κB/apoptosis signaling

“…The inflammatory cytokines are the end product of the upstream signaling proteins such as NF-κB, which are inhibited by the IκB within the cytosol [59]. During inflammatory condition, the NF-κB becomes free from the inhibitory influence of the IκB and undergoes nuclear translocation to modulate the expression of concerned genes associated with the pro-inflammatory cytokines production [59].…”

“…The inflammatory cytokines are the end product of the upstream signaling proteins such as NF-κB, which are inhibited by the IκB within the cytosol [59]. During inflammatory condition, the NF-κB becomes free from the inhibitory influence of the IκB and undergoes nuclear translocation to modulate the expression of concerned genes associated with the pro-inflammatory cytokines production [59]. Similarly, the body is armed with natural antioxidant defense mechanism such as Nrf/HO-1, which tends to neutralize the increased oxidative stress and protect the cellular environment from the oxidative stress mediated damage [60].…”

Aqueous Extract of Dacryodes edulis (Burseraceae) Leaves Inhibited Tumor Growth in Female Wistar Rats with 7,12-Dimethylbenz[a]anthracene-Induced Breast Cancer

“…e so-called phytoestrogens were reported to be able to compete with endogenous estrogens for binding estrogen receptors and to inhibit aromatase activity [51]. As recently suggested by Gul et al [44], phytoestrogenic molecules are capable of inhibiting estrogen activity (antagonistic effect against ER) or estrogen synthesis (inhibition of aromatase synthesis). e nonsignificant increase in serum levels of estradiol observed at the dose of 100 mg/kg indicates the ability of D. edulis to act in a tissue-specific way and to antagonize estrogen receptors in the mammary glands and breast tumors, thus reducing estradiol levels in these tissues, since estradiol is known to stimulate its biosynthesis in estrogen-sensitive tissues [50].…”

“…e exposition to environmental pollutants such as DMBA induced mutation, DNA damage, oncogene activation, and cancer genesis [40,41]. e administration of a single dose of DMBA (50-80 mg/kgBW) to female rats was reported to induce breast cancer development [21,[41][42][43][44]. In agreement with this report, our results showed that, after the subcutaneous administration of a single dose of DMBA (50 mg/kgBW) under the mammary gland of female Wistar rats, breast tumors developed 22-26 weeks later, with an induction percentage of 40%.…”

“…erefore, in addition to the ability of this environmental pollutant to stimulate steroidogenesis [46], DMBA may also promote the synthesis of the precursor of steroid hormones: cholesterol. e increase of estradiol levels would justify the increased invasion and density of cancer cells in breast tumors and the hypertrophy of breast lobules, taking into account the significant role of estrogens in the stimulation of cell proliferation [4,44].…”