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Cancer is one of the leading causes of death and a great threat to people around the world. Cancer treatment modalities include surgery, radiotherapy, chemotherapy, radiochemotherapy, hormone therapy, and immunotherapy. The best approach is to use a combination of several types. Among the treatment methods mentioned above, chemotherapy is frequently used, but its activity is hampered by the development of drug resistance and many side effects. In this regard, the use of medicinal plants has been discussed, and in recent decades, the use of isolated phytochemicals came into the focus of interest. By critically evaluating the available evidence and emphasizing the unique perspective offered by this review, we provide insights into the potential of daidzein as a promising therapeutic agent, as well as outline future research directions to optimize its efficacy in clinical settings. To summarized the therapeutic potential of daidzein, an isoflavone phytoestrogen in the management of several human diseases with the focuses on the current status and future prospects as a therapeutic agent. Several search engines, including PubMed, GoogleScholar, and ScienceDirect, were used, with the search terms "daidzein", "daidzein therapeutic potential", or individual effects. The study included all peer-reviewed articles. However, the most recent publications were given priority. Daidzein showed protective effects against malignant diseases such as breast cancer, prostate cancer but also non-malignant diseases such as diabetes, osteoporosis, and cardiovascular diseases. Daidzein activates multiple signaling pathways leading to cell cycle arrest and apoptosis as well as antioxidant and anti-metastatic effects in malignant cells. Moreover, the anticancer effects against different cancer cells were more prominent and discussed in detail. In short, daidzein represents a promising compound for drug development. The comprehensive potential anticancer activities of daidzein through various molecular mechanisms and its therapeutic/clinical status required further detail studies. [ABSTRACT FROM AUTHOR]

• Baicalin ameliorates insulin resistance and regulates hepatic glucose metabolism in high glucose and dexamethasone induced insulin resistant (IR)-HepG2 cells and pre-diabetic obese mice. • Baicalin treatment activates IRS/PI3K/Akt singaling pathways both in vitro and in vivo. • Baicalin reduces the expression levels of ROS and AGEs both in vitro and in vivo. Diabetes belongs to the most prevalent metabolic diseases worldwide, which is featured with insulin resistance, closely associated with obesity and urgently needs to be treated. Baicalin, belonging to natural flavonoids, has been reported to inhibit oxidative stress or inflammatoin. This study investigated the properties of baicalin on modulating abnormal glucolipid metabolism, as well as the underlying in-vitro and in-vivo mechanisms. Insulin-resistant (IR)-HepG2 cells were stimulated by dexamethasone (20 µM) and high glucose (50 mM) for 48 h and incubated with or without baicalin or metformin for another 16 h. Male C57BL/6 J mice were fed with a high-fat diet (HFD, 60 % kcal% fat) during the total 14 weeks. Obese mice were then administered with baicalin (50 and 100 mg/kg) or vehicle solution everyday through oral gavage during the last 4-week period. Moreover, baicalin metabolisms in vitro and in vivo were determined using UPLC/MS/MS to study its metabolism situation. Exposure to dexamethasone and high glucose damaged the abilities of glycogen synthesis and glucose uptake with elevated oxidative stress and increased generation levels of advanced glycation end-products (AGEs) in HepG2 cells. These impairments were basically reversed by baicalin treatment. Four-week oral administration with baicalin ameliorated hyperglycemia and dyslipidemia in HFD-induced obese and pre-diabetic mice. Downregulation of IRS/PI3K/Akt signaling pathway accomplished with reduced GLUT4 expression and enhanced GSK-3β activity was observed in insulin resistant HepG2 cells as well as liver tissues from pre-diabetic mice; and such effect was prevented by baicalin. Moreover, baicalin and its matabolites were detected in IR-HepG2 cells and mouse plasma. The study illustrated that baicalin alleviated insulin resistance by activating insulin signaling pathways and inhibiting oxidative stress and AGEs production, revealing the potential of baicalin to be a therapeutic natural flavonoid against hepatic insulin and glucose-lipid metabolic disturbance in pre-diabetes accompanied with obesity. [Display omitted] [ABSTRACT FROM AUTHOR]

6-benzylaminopurine (6-BA), classified as a "plant hormone", is an important ingredient in production of "toxic bean sprouts". Although there is no direct evidence of adverse effects, its hazardous effects have received some attention and aroused furious debate between proponents and environmental regulators. In this study, potential adverse effects of 6-BA were investigated by exposing zebrafish in vivo to 0.2 – 25 mg 6-BA/L. Results indicated that, when exposure was limited to early-life stage (4–36 hpf), 20 mg 6-BA/L caused early hatching, abnormal spontaneous movement, and precocious hyperactivity in zebrafish embryos/larvae. While under a continuous exposure regime, 6-BA at 0.2 mg/L was able to cause hyperactive locomotion and transcription of genes related to neurogenesis (gnrh3 and nestin) and endocrine systems (cyp19a and fshb) in 5 dpf larvae. Quantification by use of LC/MS indicated bioaccumulation of 6-BA in zebrafish increased when exposed to 0.2 or 20 mg 6-BA/L. These results suggested that 6-BA could accumulate in aquatic organisms and disrupt neuro-endocrine systems. Accordingly, exposure to 0.2 mg 6-BA/L increased production of estradiol (E2) and consequently E2/T ratio in zebrafish larvae, which directly indicated 6-BA is estrogenic. In silico simulations demonstrated potential for binding of 6-BA to estrogen receptor alpha (ERa) and cytochrome P450 aromatase (CYP19A). Therefore, induction of estrogenic effects, via potential interactions with hormone receptors or disturbance of downstream transcription signaling, was possible mechanism underlying the toxicity of 6-BA. Taken together, these findings demonstrate endocrine disrupting properties of 6-BA, which suggest concerns about risks posed to endocrine systems. [Display omitted] • 6-BA caused earlier hatching and precocious hyperactivity in zebrafish. • 6-BA elicited expression of endocrine disrupting and neurogenesis genes in zebrafish. • 6-BA is estrogenic in zebrafish larvae through increased production of estradiol (E2). • In vivo exposure of zebrafish to 6-BA might be hazardous via endocrine disruption. [ABSTRACT FROM AUTHOR]