1. Quercetin is one of the most prominent dietary antioxidants, it is claimed to exert beneficial health effects, this includes protection against various diseases such as osteoporosis, certain forms of cancer, pulmonary and cardiovascular diseases but also against aging.
2. Quercetin aglycone modulates several signal transduction pathways involving MEK/ERK and Nrf2/keap1, which is associated with the processes of inflammation and carcinogenesis.
3. Guercetin can attenuate the function of AR by repressing its expression, inhibit the secretion of the prostate-specific, androgen-regulated tumor markers, PSA and hK2. and has the potential to become a chemopreventive and/or chemotherapeutic agent for prostate cancer.
4. Quercetin and curcumin modulate ACFs correlates well with their ability to induce apoptosis via the mitochondrial pathway, may exert significant and potentially beneficial effects on decreasing the amount of precancerous lesions and inducing apoptosis in the large intestine.
5. Quercetin supplementation reduces blood pressure in hypertensive subjects.
1. Alpha-lipoic acid has become a common ingredient in multivitamin formulas, anti-aging supplements, and even pet food, it is well-defined as a therapy for preventing diabetic polyneuropathies, and scavenges free radicals, chelates metals, and restores intracellular glutathione levels which otherwise decline with age.
2. Alpha-lipoic acid can enhance glucose transport and utilization in different experimental and animal models, it can improve insulin sensitivity in patients with type-2 diabetes.
3. Lipoic acid is a novel treatment for Alzheimer's disease and related dementias.
4. Alpha-lipoic acid has therapeutic effects on joint inflammation and erosion in an animal model via NF-kappa B down regulation, it inhibits TNF-alpha induced NF-kappa B activation through blocking of MEKK1-MKK4-IKK signaling cascades.
1. Cycloastragenol and astragaloside IV can suppress ROS-associated ER stress and then inhibit TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorate endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis.
2. Cycloastragenol stimulates telomerase activity in human neonatal keratinocytes and rat neuronal cells, and induces CREB activation followed by tert and bcl2 expression, cycloastragenol may have a novel therapeutic role in depression.
3. Cycloastragenol can suppress the accumulation of cytoplasmic lipid droplet in 3T3-L1 adipocytes.
4. Cycloastragenol and astragaloside IV have been shown to improve the proliferative response of CD8+ T lymphocytes from HIV-infected patients by upregulating telomerase activity, they also may exert their cellular effects through the activation of the Src/MEK/ERK pathway.
5. Cycloastragenol can remarkably inhibit CYP3A4 and activate CYP2E1 in rats.
6. Cycloastragenol has been shown to extend T cell proliferation by increasing telomarase activity showing that it may also help delay the onset of cellular aging; it is an extraordinary wound healing agent; it inhibits the apoptosis of PC12 induced by 6-OHDA, may be as potential neuroprotective agents in the treatment of Parkinson's disease.
1. Epifriedelanol can suppress adriamycin-induced cellular senescence as well as replicative senescence in human fibroblasts (HDFs) and human umbilical vein endothelial cells (HUVECs), suggests that epifriedelanol can reduce cellular senescence in human primary cells and may be used to develop dietary supplements or cosmetics that modulate tissue aging or aging-associated diseases.
2. Epifriedelanol exhibits significant inhibition of NF-kappa B, it may be used to treat asthma.
3. Epifriedelanol has antitumor activity.
1. Nicotinamide may be used as a substrate of nicotinamide phosphoribosyltransferase , the rate-limiting enzyme for NAD(+) biosynthesis and an important signaling molecule.
2. Nicotinamide is a building block of coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phopshate (NADP).