Asiaticoside from Gotu kola reverses senescence and oxidative damage in blood vessels

“TL;DR: Asiaticoside, an active from gotu kola / centella asiatica, has been found to reverse oxidative damage and senescence in endothelial (blood vessel lining) cells.

Cellular senescence of the adipose tissue, connective tissue and blood vessels is an important and largely unexplored cause of cellulite. Oxidative damage is an established cause of cellulite.”

The Centella asiatica active Asiaticoside eliminates free radical damage in blood vessels

• Asiaticoside from Gotu Kola prevents oxidative damage and reverses all markers of oxidation in endothelial cells

• In addition, asiaticoside partially reverses cell senescence

• Asiaticoside in cellulite creams and nutritional supplements

• Asiaticoside Prevents Oxidative Stress and Apoptosis in Endothelial Cells by Activating ROS-dependent p53/Bcl-2/Caspase-3 Signaling Pathway

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Asiaticoside from Gotu Kola prevents oxidative damage and reverses all markers of oxidation in endothelial cells

Asiaticoside and the other three centella asiatica main active molecules (asiatic acid, madecassic acid, asiaticoside and madecassoside) are known for their multiple action against whole body ageing, skin ageing and cellulite.

In this new study of human umbilical vein endothelial cells (HUVECs), asiaticoside was found to reverse all markers of oxidative stress.

Furthermore, asiaticoside restored antioxidant markers, such as SOD (superoxide dismutase), NO (nitric oxide) and GSH-Px (glutathione peroxidase), after oxidative insult.

In addition, asiaticoside partially reverses cell senescence

Plus asiaticoside significantly reversed senescence-associated beta-galactosidase (SA-β-gal) activity, a marker of cell senescence. (Senescence is a major cause of ageing and whole body inflammation - and consequently cellulite.)

Given its anti-senescence properties, asiaticoside can be used as part of anti-senescence / senolytic regime for blood vessels and entire body.

Asiaticoside in cellulite creams and nutritional supplements

Cellular senescence is an important aspect of cellulite, especially senescence of blood vessels, skin and adipose tissue. Asiaticoside, and most probably the other three gotu kola triterpenes too, help reverse senescence.

Furthermore, gotu kola helps fight cellulite via multiple other pathways, including fibrosis, inflammation, glycation and oxidative stress reduction.

So the anti-senescence action of asiaticoside, adds yet another way in which gotu kola / centella asiatica helps prevent / reduce cellulite.

Asiaticoside can be found in:

• Proper, therapeutic concentrations in a very small number of quality anti-cellulite and anti-aging creams (most are very diluted and/or contain low purity active ingredients)

• A small number of quality centella asiatica / gotu kola nutritional supplements (difficult to source and most are not concentrated enough)

• Centella asiatica herbal tea (easy to source on the internet these days)

Asiaticoside Prevents Oxidative Stress and Apoptosis in Endothelial Cells by Activating ROS-dependent p53/Bcl-2/Caspase-3 Signaling Pathway

• Link: https://www.eurekaselect.com/article/127161

• Abstract: Background: Asiaticoside (AC) is a triterpenoid saponin found in Centella asiatica (L.) Urban extract that has a wide range of pharmacological properties. Our previous study demonstrated that AC could promote angiogenesis in diabetic wounds, but the specific mechanisms remain unknown. Objective: This study aimed to examine the effectiveness and mechanism of AC on human umbilical vein endothelial cells (HUVECs) exposed to tert-butyl hydroperoxide (t-BHP) toxicity. Methods: Senescence was confirmed using senescence-associated beta-galactosidase (SA-β-gal) activity and expression of the cell cycle phase markers p16 and p21. The levels of SOD, NO, MDA, GSH-Px, ROS were tested. Furthermore, several cell death-related genes and proteins (p53, Bax, Bcl-2 and Caspase-3) were assessed with RT-qPCR and Western blotting. Results: AC significantly reduced SA-β-gal activity, with both the suppression of cell-cycle inhibitors p16 and p21. We also found that the induced oxidative stress and apoptosis caused by t-BHP treatment resulted in the decrease of antioxidant en-zymes activities, the surge of ROS and MDA, the up-regulation of p53, Bax and caspase-3, and the decrease of SOD, NO, GSH-Px and Bcl-2. These biochemical changes were all reversed by treatment with varied doses of AC. Conclusion: AC alleviates t-BHP-induced oxidative injury and apoptosis in HUVECs through the ROS-dependent p53/Bcl-2/Caspase-3 signaling pathway. It may be a potential antioxidant applied in metabolic disorders and pharmaceutical products.

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