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Selected Botanicals and Plant Products That Lower Blood Glucose (Continued)
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
Silymarin (mixture) at 50 μM has been shown to accumulate daunomycin, the substrate of P-glycoprotein (P-Gp), in cells expressing P-Gp, with no effect on cells that do not express P-Gp. This study noted accumulation of 445% ± 12%, which was similar to phloretin and slightly less than Morin (from Morus alba) and Biochanin A (Zhang, and Morris. 2003). Silymarin did not appear to influence the protein content of P-Gp, did not interact with the ATPase activity of P-Gp, and inhibited vermapril-induced ATPase activity on P-Gp; the inhibition at 100 μM reaches 61.2% ± 20.7% in vitro, comparable to that of vinblastine (Zhang, and Morris. 2003).
Dietary Phytoestrogens
Published in Rajesh K. Naz, Endocrine Disruptors, 2004
Heather B. Patisaul, Patricia L. Whitten
The isoflavonoids are divided into three major classes: isoflavones, isoflavans, and coumestans, of which the isoflavones are the most widely studied group. The major mammalian isoflavones are genistein and daidzein, which are formed from the plant precursors formononetin and biochanin A, respectively. The most significant isoflavan is equol, a metabolite of daidzein. Coumestrol is the major coumestan. Very little is known about the coumestans compared to the other isoflavonoids. Coumestrol is the most potent phytoestrogen, with a binding affinity similar to 17β-estradiol for ERα and an affinity nearly twice that of 17β-estradiol for ERβ.10
Bladder and Prostate Cancer
Published in Spyridon E. Kintzios, Maria G. Barberaki, Evangelia A. Flampouri, Plants That Fight Cancer, 2019
Charlie Khoo, Yiannis Philippou, Marios Hadjipavlou, Abhay Rane
Research to date has mainly focused on biochanin-A and formononetin, two of the major isoflavones found in red clover. Biochanin-A has been shown to induce apoptosis in vitro in prostate cancer cell lines (Hempstock et al. 1998, Peterson and Barnes 1993). Tumor necrosis factor related apoptosis inducing ligand (TRAIL) is cleaved from the surface of immune cells. It binds to death receptors (DRs) on the surface of cancer cells, inducing apoptosis. Szliska et al. incubated prostate cancer cell lines with biochanin-A, TRAIL, and the two in combination. Both alone were effective in inducing apoptosis compared to control, however, the combined treatment significantly enhanced apoptosis compared to either agent alone. Biochanin-A was found to up-regulate expression of DRs in prostate cancer cells and also inhibit transcription factor NF-кB (which protects tumor cells from apoptosis) (Szliszka et al. 2013). Formononetin is effective against human prostate cancer cell lines in vitro compared to control (Liu et al. 2014, Ye et al. 2012, Zhang et al. 2014). There are a number of proposed mechanisms. Formononetin upregulates expression of RASD1, a gene implicated in regulating cell differentiation (Liu et al. 2014). Western blot analysis has also shown that formononetin inhibits production of Bcl-2 (an anti-apoptotic protein) whilst increasing production of Bax (a pro-apoptotic) (Zhang et al. 2014). Furthermore, it also inactivates the extracellular signal regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) pathway (known to regular cellular mitosis) (Ye et al. 2012).
Investigation of apoptotic and antiproliferative effects of Turkish natural tetraploids Trifolium pratense L. extract on C6 glioblastoma cells via light and electron microscopy
Published in Ultrastructural Pathology, 2023
Gamze Tanrıverdi, Aynur Abdulova, Hatice Çölgeçen, Havva Atar, Belisa Kaleci, Tuğba Ekiz-Yılmaz
Therefore, the aim of this study was to reveal the efficacy and the possible antitumoral effects of Turkish natural tetraploid Trifolium pratense L. extract on C6 Glioblastoma cells. For this purpose, five different concentrations of this extract were applied to C6 cells for promoting cell death and were tested in an in vitro model. At the end of 24 h and 48 hours incubation time, the plant extract reduced the CCK-8 index in all the different dose groups compared to the control group. IC50 values of the experimental doses were as followed: 12.5 µg/mL in 24 h, 12.5 µg/mL and 25 µg/mL in the 48 h, in the experimental groups, respectively. Apoptotic markers had highest levels on the same doses. These results showed that the Turkish natural tetraploid Trifolium pratense L. extract decreased cell proliferation and induced apoptosis in a time and dose-dependent manner. In a similar study, Khazaei M et al., applied Trifolium pratense L. hydroalcoholic extract together with TMZ and reported that there had been a significant synergy between these two agents and they had decreased cell proliferation and induced apoptosis.33 Sehm et al. also studied the biochanin A and genistein isoflavones, provided from Trifolium pratense L. and found out about their inhibitory effects on U251 glioma cells proliferation and the enhancing apoptotic effects on the same cells.34 In addition, Li Y et al. reported that biochanin A has been effective on lung cancer cells via cell cycle arrest and increasing apoptotic markers like caspase-3, p21, and bcl-2.35
Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasome
Published in Pharmaceutical Biology, 2022
A large amount of data showed that inflammation can aggravate myocardial I/R injury, so many pharmacological studies are focussed on inhibiting the inflammatory response in exploring the reduction of I/R injury (Rameshrad et al. 2016; Kosuru et al. 2018). For example, Bai et al. (2019) demonstrated that biochanin A alleviated I/R by reducing the expression of inflammatory cytokines IL-1β and IL-18. Consistently, we also found that didymin reduced the levels of the above-mentioned inflammatory factors in myocardial tissue and cells. NLRP3 inflammasome is a participant of inflammatory immune response, consisting of NLRP3, ASC and pro-caspase-1 precursor, which has been confirmed to be involved in the occurrence and development of myocardial I/R injury (Luo et al. 2017; Yue et al. 2019). After NLRP3 is activated, it binds to ASC and further activates caspase-1. Then, the activated caspase-1 continues to cleave the precursors of IL-1β and IL-18 as active cytokines, which are involved in the development of inflammation and myocardial I/R injury. Kawaguchi et al. (2011) demonstrated that NLRP3 was activated and promoted inflammatory cytokine release during I/R. In addition, Wang et al. (2020) reported that artemisinin alleviated myocardial injury by inhibiting NLRP3 inflammasome activation. As expected, our data suggested that NLRP3, ASC, IL-1β and IL-18 expression increase after I/R injury, while didymin treatment inhibited NLRP3 inflammasome activation and inflammatory response.
Aggravated behavioral and neurochemical deficits and redox imbalance in mice with enhanced neonatal iron intake: improvement by biochanin A and role of microglial p38 activation
Published in Nutritional Neuroscience, 2021
Yunhong Li, Ying Liu, Yaling Xu, Hanqing Chen, Zhiqiang Yan, Xijin Wang
In this study, C57BL/6 mice pups with enhanced iron (120 µg/g bodyweight) intake in the neonatal period were administered MPTP (12 mg/kg) for 4 days when they were aged to 98 days. We investigated the joint effect of iron and MPTP and possible mechanisms for action on behavioral and neurochemical indicators in the mice. Biochanin A (C16H12O5, BA) is a naturally occurring isoflavone that is most commonly found in legumes, such as peanuts, alfalfa sprouts, soy, and red clover. As an O-methylated isoflavone, BA could exhibit antioxidant properties [12]. It has been reported that BA protects neurons against lipopolysaccharide-induced damage through repressing proinflammatory factors generation [13]. Therefore, we also explored the effect of BA oral administration and possible mechanism for action in the mice with the co-administration of iron and MPTP in this study. Finally, further mechanism was investigated through in vitro experiments in our study.