Group items tagged

uring days 15–28, pigs in the CHE group had lower (P < .05) diarrhoea frequency compared with those in the NC treatment, and dietary CHE supplementation decreased the diarrhoea frequency by 63.62% and 57.82% compared with the NC and PC groups, respectively

Furthermore, pigs in the CHE group had greater (P < .05) formic acid, propionate and butyrate concentrations in faeces compared with pigs in the PC group, and had greater (P < .05) formic acid, butyrate and valerate concentrations in faeces compared with pigs in the NC group

Pigs in the CHE group showed increased relative abundance of Sytrophococcus on genus level, and decreased (P < .05) relative abundance of Clostridiaceae_1

but decreased the incidence of diarrhoea and increased digestibility of some nutrients.

With DRE having proven its efficacy in successfully killing this aggressive, chemoresistant form of skin cancer, DRE toxicity on normal cells had to be evaluated

After a long exposure of 96 hours, NHFs did not exhibit any reduction in cell viability

Higher doses were then used and a response was observed at a concentration of 10 mg/mL (

Typical apoptotic morphology was observed in G361 cells treated with DRE starting at 5 mg/mL concentrations for 72 hours

) is more than a worthy chemopreventative, it is fast-acting, nontoxic, and therefore specific in its targeting of human melanoma cancer cells, making it a valuable chemotherapeutic. We have investigated the induction of apoptosis in human malignant melanoma cells and observed its long-term effects in human melanoma cancer.

By 48 hours, human melanoma A375 cells uncharacteristically showed susceptibility to apoptosis induction by DRE

Given that DRE has traditionally been used naturopathically for a variety of ailments, we assume that it would be relatively nontoxic to healthy cells. Our results show that the Normal Human Fibroblasts (NHFs) (which were treated at a low population doubling where NHFs have the best proliferation rate) and Peripheral Blood Mononuclear Cells remained unaffected and healthy after a 96-hour and 48- hour exposure to DRE, respectively (Figures 2(a)–2(d)).

Lupeol,

taraxasterol

More importantly, an increase in ROS production indicates prooxidant behaviour of DRE on cancer cell mitochondria, which is contrary to the antioxidant convictions of traditional medicine and previous studies on Taraxacum extracts citing reductions in NO, ROS, RNS, and COX-2 [10, 11] in mouse macrophages.

There are two main points that must be stated here: firstly, that noncancerous cells are unaffected by DRE treatment, and secondly, melanoma cells retain the signals to commit suicide long after DRE has been removed from the system

We are yet to determine the effect of each of the individual components (such as the family of triterpene alcohols and phenolic acids—found in the roots—and cinnamic acids, flavinoids and coumarins—that are found in the leaves

We believe that this nontoxic extract can undergo precipitous translation from bench top to bedside, with dandelion products that are already commercially available in the form of tea and supplements.

γ rays

This review specifically focuses a current understanding on the dietary sources of polyphenols and their protective effects including mechanisms of action against various major human diseases.

ROS when increased or excessively produced can cause oxidative changes/damages to all cellular macromolecules

Several antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) aid in the removal of free radicals

Peroxynitrite can also destroy lipoproteins and causes lipid peroxidation of cell membranes

ROS can also affect protein synthesis and protein functions. Protein oxidation can result in amino acid modifications

Flavonoids are further classified into different subgroups based on their structures such as flavan-3-ols (examples: catechin, epicatechin, epigallocatechin), isoflavones (examples: genistein, genistin, daidzenin, daidzin, biochanin A, formononetin), flavones (examples: luteolin, apigenin, chrysin), flavonones (examples: hesperetin, naringenin), flavonols (examples: quercetin, kaempferol, galangin, fisetin, myricetin), flavononol (example: taxifolin), flavylium salts (examples: cyanidin, cyanin, pelargonidin), and flavanones (examples: hesperetin, naringenin, eriodictyol, isosakuranetin)

urther, OS exerts deleterious effects on DNA leading to the formation of DNA lesions, which can result in genomic instability and consequently lead to cell death.

Polyphenols are found naturally in fruits and vegetables such as cereals, pulses, dried legumes, spinach, tomatoes, beans, nuts, peppermint, cinnamon, pears, cherries, oranges, apples, red wine, tea, cocoa, coffee and so on (Arts and Hollman, 2005; Scalbert et al., 2005). Polyphenols are classified into different groups depending on the number of aromatic (phenolic) rings they contain and the structural elements that connect these rings. They are broadly grouped into phenolic acids, flavonoids, stilbenes and lignans

Dietary supplements containing elevated amounts of flavonoids from strawberries, lettuce, or blueberries aid in the reversal of age-related discrepancies in the brain and behavioral control in aged rats

Tea catechins

OS can be the primary or secondary reason for various CVDs. Preclinical evidence support that OS is linked to a variety of CVDs, including atherosclerosis, ischemia, stroke, cardiomyopathy, cardiac hypertrophy, and hypertension, as well as congestive heart failure

Dietary flavonoids may reduce endothelial disorders linked with various risk factors for atherosclerosis before plaque creation

The polyphenols of Hibiscus sabdariffa weaken diabetic nephropathy in terms of serum lipid profile and kidney oxidative markers

. Studies suggest that a diet that includes regular consumption of fruits and vegetables (rich in polyphenols such as catechins, resveratrol, ellagic acid, naringenin, quercetin etc.) significantly lowers the risk of developing many cancers.

Black tea polyphenols like EGCG, theaflavins and thearubigins have potent anticancer properties

Increased OS may lead to the vulnerability of the infection and also triggers the malfunctioning of cellular metabolism

In this line of research, novel therapies aim to target apoptosis via mitochondria, using molecules that mimic BH3 proteins and disrupt the interactions of pro-apoptotic and anti-apoptotic proteins.

Therefore, the mechanisms by which mushroom extracts or isolated compounds induce mitochondrial-related apoptosis pathways are diverse and may be related with specific bioactive compounds. Modulation of pathways crucial for cell survival and alterations in lipid homeostasis seem to be related with the pro-apoptotic effects observed in HCC cell lines and in in-vivo xenograft models.

To sum up, mitochondria play a central role in the pathophysiology and progression of NAFLD as well as in the development of HCC, which can be a late-stage consequence of NASH. Hepatic mitochondria undergo bioenergetic remodelling to face the metabolic burden imposed by the increased FFAs load secondary to systemic IR. In turn, a decompensation of these processes may result in ROS formation and mitochondrial dysfunction, contributing to the development of NASH. Lastly, hepatic mitochondria also seem to be involved in anti-apoptotic oncogenic processes driving HCC. Targeting mitochondrial dysfunction is thus a promising approach for the treatment of the NAFLD continuum. The following section describes some of the in-vitro and in-vivo studies on the beneficial effects of mushroom-enriched diets or mushroom-derived compounds/extracts (Box 2) in preventing/reverting such liver damage.