Background: Cancer stemcellsareasubpopulationoftumorcellsthatarecapableofself-renewal,capableoftumor recurrence andmetastasis,andinadditionareresistanttocurrentcancertherapies.Epigallocatechin-3-gallateisatypeof catechin foundingreenteathatisknownforitspowerfulchemoprotectiveability.Hence,thisstudyaimedtoinvestigatethe effect ofepigallocatechin-3-gallateon7,12dimethylbenzanthracene-inducedtumormetastasis,angiogenesisandcancer stem cells. Materials andMethods: For thispurpose,3groupsofvirginfemalratswith7,12dimethylbenzanthracene-induced mammary cancerweretreatedusingepigallocatechin-3-gallate,paclitaxelortheircombination. Results: It wasfoundthatepigallocatechin-3-gallateexhibitedsignificant chemopreventiveeffectsandanti-cancerstemcell activity throughseveralpathways,includingasignificant decreaseinthesizeandnumberoftumorsperrat,significant amelioration oftheoxidativestressmarkers’ alterations andsignificant inhibitionofCD44,VEGF,Ki-67andMMP-2 expression associatedwithasignificantly increasedexpressionofcaspase-3.Histopathologically,therapywithepigalloca- techin-3-gallate resultedinmarkednecrosisoftheneoplasticcellsandthetumormassesweremostlyreplacedby proliferated fibrous tissuesothathistologicalconfirmation ofaprevioustumorwasnotpossibleatthatsite.However,inthe combination therapytheneoplasticcellsshowedmarkedvacuolation,haphazardarrangementandextensivenuclear pyknosis accompaniedwithmanyapoptoticbodies.Therapywiththesolepaclitaxelcausedvariabledegreesofnecrosis among theneoplasticcells.Additionally,thecombinationofepigallocatechin-3-gallateandpaclitaxelsignificantly enhanced the lateranticancerefficacy. Conclusions: Epigallocatechin-3-gallatecould beofferedasanunprecedentedcurativestrategytoeradicatecancer
Abstract: Ferritin is a shell-like carrier protein with an 8nm diameter cavity which endows a natural space to encapsulate food and drug components. In this work, phytoferritin was unprecedentedly glycosylated by chitosan to fabricate ferritin-chitosan Maillard reaction products (FCMPs) (grafting degree of 26.17%, 24h, 55°C). Results indicated that the amide I and II bands of ferritin were altered due to the chitosan grafting, whereas the ferritin spherical structure were retained. Simulated digestion analysis showed that the FCMPs were more resistant to pepsin and trypsin digestion as compared with ferritin alone. Furthermore, FCMPs were employed as carrier to encapsulate epigallocatechin gallate (EGCG) molecules with an encapsulation ratio of 12.87% (w/w), and the resulting FCMPs-EGCG complexes showed a slow release of EGCG in simulated gastrointestinal tract. Interestingly, different types of food components displayed different effects in EGCG release behavior from the FCMPs, wherein proanthocyanidin, milk and soy protein inhibited the EGCG release. In addition, the absorption of EGCG encapsulated in FCMPs in Caco-2 monolayer model was significantly improved as compared with free EGCG. This work provides a novel nano-vehicle for fabricating core-shell systems in food and drug delivery domain.
Pub.: 12 Jul '17, Pinned: 08 Aug '17
Abstract: Activation of nuclear factor erythroid 2-related factor 2 (NRF2) has been found to ameliorate diabetic testicular damage (DTD) in rodents. However, it was unclear whether NRF2 is required for these approaches in DTD. Epigallocatechin gallate (EGCG) is a potent activator of NRF2 and has shown beneficial effects on multiple diabetic complications. However, the effect of EGCG has not been studied in DTD. The present study aims to explore the role of NRF2 in both self and EGCG protection against DTD. Therefore, streptozotocin-induced diabetic C57BL/6 wild type (WT) and Nrf2 knockout (KO) mice were treated in the presence or absence of EGCG, for 24 weeks. The Nrf2 KO mice exhibited more significant diabetes-induced loss in testicular weight and spermatozoa count, and increase in testicular apoptotic cell death, as compared with the WT mice. EGCG activated NRF2 expression and function, preserved testicular weight and spermatozoa count, and attenuated testicular apoptotic cell death, endoplasmic reticulum stress, inflammation, and oxidative damage in the WT diabetic mice, but not the Nrf2 KO diabetic mice. The present study demonstrated for the first time that NRF2 plays a critical role in both self and EGCG protection against DTD.
Pub.: 13 Jul '17, Pinned: 08 Aug '17
Abstract: Obesity, which is caused by an energy imbalance between calorie intake and consumption, has become a major international health burden. Obesity increases the risk of insulin resistance and age-related cognitive decline, accompanied by peripheral inflammation. (-)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, possesses antioxidant, anti-inflammatory, and cardioprotective activities; however, few reports have focused on its potential effect on cognitive disorders. In this study, our goal was to investigate the protective effects of EGCG treatment on insulin resistance and memory impairment induced by a high-fat and high-fructose diet (HFFD). We randomly assigned 3-mo-old C57BL/6J mice to 3 groups with different diets: control group, HFFD group, and HFFD plus EGCG group. Memory loss was assessed by using the Morris water maze test, during which EGCG was observed to prevent HFFD-elicited memory impairment and neuronal loss. Consistent with these results, EGCG attenuated HFFD-induced neuronal damage. Of note, EGCG significantly ameliorated insulin resistance and cognitive disorder by up-regulating the insulin receptor substrate-1 (IRS-1)/AKT and ERK/cAMP response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathways. Long-term HFFD-triggered neuroinflammation was restored by EGCG supplementation by inhibiting the MAPK and NF-κB pathways, as well as the expression of inflammatory mediators, such as TNF-α. EGCG also reversed high glucose and glucosamine-induced insulin resistance in SH-SY5Y neuronal cells by improving the oxidized cellular status and mitochondrial function. To our knowledge, this study is the first to provide compelling evidence that the nutritional compound EGCG has the potential to ameliorate HFFD-triggered learning and memory loss.-Mi, Y., Qi, G., Fan, R., Qiao, Q., Sun, Y., Gao, Y., Liu, X. EGCG ameliorates high-fat- and high-fructose-induced cognitive defects by regulating the IRS/AKT and ERK/CREB/BDNF signaling pathways in the CNS.
Pub.: 26 Jul '17, Pinned: 08 Aug '17
Abstract: Hydrogen sulphide (H2S) is a colourless gas with the odour of rotten eggs and has recently been recognized as a signal mediator in physiological activities related with the regulation of homeostasis, the vascular system and the inflammatory system. Here we show that H2S donors, including sodium hydrogen sulphide (NaHS), GYY 4137 and diallyltrisulfide (DATS), synergistically enhanced the anti-cancer effect of a green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) against multiple myeloma cells without affecting normal cells. NaHS significantly potentiated the anti-cancer effect of EGCG and prolonged survival in a mouse xenograft model. In this mechanism, H2S enhanced apoptotic cell death through cyclic guanosine monophosphate (cGMP)/acid sphingomyelinase pathway induced by EGCG. Moreover, NaHS reduced the enzyme activity of cyclic nucleotide phosphodiesterase that is known as cGMP negative regulator. In conclusion, we identified H2S as a gasotransmitter that potentiates EGCG-induced cancer cell death.
Pub.: 29 Jul '17, Pinned: 08 Aug '17
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