The Potential of Using Cochayuyo (Durvillaea incurvata) Extract Obtained by Ultrasound-Assisted Extraction to Fight against Aging-Related Diseases

Abstract

The world’s population is in a demographical transition, with an increase in the number of older adults and prevalence of diseases related to aging. This study evaluated in vitro the potential of using Durvillaea incurvata extract (extracted using ultrasound-assisted extraction) to inhibit key enzymes associated with the development of age-related diseases. Our results show that an extract extracted via ultrasound-assisted extracted, as well as an extract conventional extracted from Durvillaea incurvata, presented antidiabetes potential by exhibiting inhibitory activity against α-glucosidase (91.8 ± 1.0% and 93.8 ± 0.3%, respectively, at 500 µg/mL) and α-amylase (42.2 ± 1.4% and 61.9 ± 0.9%, respectively, at 1500 µg/mL) enzymes related to starch digestion and postprandial glycemic response. Also, the extracts showed inhibitory activity against the enzymes acetylcholinesterase (51.5% and 50.8%, respectively, at 500 µg/mL) and butyrylcholinesterase (32.8% and 34.4%, respectively, at 0.5 mg/mL), the biomarkers associated with Alzheimer’s disease, and angiotensin-converting enzyme (98.7 ± 7.4% and 93.0 ± 3.4%, respectively, at 2.0 mg/mL), which is key in the regulation of vascular tone and blood pressure and helps to prevent the development of hypertension. In conclusion, the extract of Durvillaea incurvata obtained from ultrasound-assisted extraction has the potential to prevent the development of age-related pathologies such as diabetes, Alzheimer’s disease, and hypertension.

Current Research On Epigenetic Age and Cellular Senescence: A Bibliometric and Visual Analysis

“…DNA methylation has received great attention in the study of genetic epigenetic age and cellular senescence, mainly due to the role it plays in the study of genetic epigenetic age and cellular senesce nce through various modifications of oxidative stress, DNA damage, Telomere changes and SASP development in cellular senescence [34]. For example, the cell cycle is regulated by changes in DNA methylation levels during telomere shortening [35]., which can affect t elomere length and integrity to regulate cellular senescence, leading to DNA da mage and promoting p53/p21 expression [36].During SASP secretion, DNA met hylation affects the inflammatory process mainly by regulating the expression o f pro-and anti-inflammatory cytokines [37], which in turn affect the cell cycle by regulating p53/p21 and p16 expression, thereby influencing the progression of cellular senescence [38].During DNA damage, methylation modifications regu late cellular senescence by influencing DNA polymerase recruitment at damage sites and regulating DNA break repair to regulate p53/p21 expression [39].Duri ng oxidative stress, methylation mainly acts on oxidative and antioxidant syste ms to regulate oxidative and antioxidant homeostasis in vivo [40].…”

“…, which can affect telomere length and integrity to regulate cellular senescence, leading to DNA da mage and promoting p53/p21 expression [36]. During SASP secretion, DNA methylation affects the inflammatory process mainly by regulating the expression of pro- and anti-inflammatory cytokines [37], which in turn affect the cell cycle by regulating p53/p21 and p16 expression, thereby influencing the progression of cellular senescence [38]. During DNA damage, methylation modifications regulate cellular senescence by influencing DNA polymerase recruitment at damage sites and regulating DNA break repair to regulate p53/p21 expression [39].…”