Urolithin A Powder

Urolithin A powder is a natural polyphenolic compound, chemically named 3,8-dihydroxy-6H-dibenzo[B,D]pyran-6-one, produced by the metabolism of ellagic acid through intestinal flora. It appears as a white to pale yellow crystalline powder and possesses various biological activities, including antioxidant, anti-inflammatory, anti-proliferative, and mitophagy-activating effects.

Studies have shown that urolithin A is one of the few known natural molecules capable of inducing the selective clearance of damaged mitochondria via autophagy while simultaneously promoting the biosynthesis of healthy mitochondria. It can cross the blood-brain barrier and exert neuroprotective effects, showing clear application potential in aging intervention, prevention of neurodegenerative diseases, and adjunctive intervention for sarcopenia.

YTBIO is a supplier and manufacturer of Urolithin, mainly supplying Urolithin A and Urolithin B with a specification of 98%. All the products we supply have been tested and support third-party testing. In the ten years of development in the industry, we have accumulated global customers and gained recognition from customers. If you need a supplier with certain strength, I think YTBIO is a good choice.

1. Urolithin A improves mitochondrial and muscle function, improving muscle strength and endurance during aging.
Urolithin A alleviates muscle atrophy in the elderly. This experiment demonstrates that urolithin A supplementation can enhance muscular endurance of skeletal muscles, with significant improvements in the hands and legs of the subjects.

2. Not only can it protect muscles, the latest research has found that urolithin A can actually affect cellular lipid metabolism and fat production. It reduces triglyceride accumulation and fatty acid oxidation, as well as the expression of genes involved in lipogenesis.

3. Protection against muscle loss is a recent discovery, and previous research on it has focused on mitochondria, especially mitophagy. (Mitophagy refers to the selective removal of damaged mitochondria by autophagosomes)
UA can activate mitophagy in a variety of ways, such as activating enzymes that promote mitophagy, or regulating the mitophagy pathway, and promoting the formation of autophagosomes.

4. Among all clinical models of UA, there is a common effect, which is the weakening of inflammatory response.

This effect was first discovered when both the mRNA and protein levels of the inflammatory marker cyclooxygenase 2 were reduced in intestinal inflammation experiments in rats.

With more research, it was found that other inflammatory markers, such as pro-inflammatory factors, also decreased to varying degrees.
The anti-inflammatory effect of UA is multi-faceted. First of all, it exists in large quantities in the intestinal tract, so the most effective is inflammatory bowel disease. Including acute enteritis, ulcerative colitis.

Second, UA not only protects against intestinal inflammation, because it reduces the overall serum levels of inflammatory factors. In theory, UA can work on diseases caused by inflammation.

When UA exerts anti-inflammatory effects in the brain, it can improve many neurodegenerative diseases, including Alzheimer's disease (AD), memory impairment and stroke.

5. In fact, the anti-inflammatory and mitophagy activation of urolithin A can already slow down the symptoms of metabolic diseases. But it also has a powerful effect, which is to improve oxidative stress, not only to scavenge free radicals, but also to inhibit oxidase enzymes, and to enhance cellular antioxidant/source.

Many medical experts believe that the beneficial properties of UA are due to the antioxidant capacity of UA.

Promoting selective autophagy of damaged mitochondria and restoring mitochondrial dysfunction caused by aging are the main regulatory mechanisms of UA found in many species (nematodes, mice, humans, etc.). When mitochondria are exposed to external stress and damaged, autophagy theoretically begins. UA essentially acts as an autophagy inducer and mainly participates in and regulates the mitophagy process through two pathways:

PINK1/Parkin ubiquitin-dependent pathway
In the ubiquitin-dependent pathway of mitophagy, after PINK1 protein recognizes target mitochondria, it recruits and phosphorylates the ubiquitin-binding protein Parkin, jointly promoting the ubiquitination of mitochondrial proteins, amplifying autophagy signals, and "rushing" to phagocytes. UA activates the expression of related genes, upregulates the levels of PINK1 and Parkin proteins, and promotes the mitochondrial autophagy process.

direct receptor activation pathway
In addition to relying on the PINK1/Parkin pathway, mitochondria can also "change paths" to utilize certain receptor proteins (such as BNIP3) to directly activate the autophagy process. UA "will never abandon and function stably", upregulating the expression level of receptor proteins. making it easier to accumulate on the mitochondrial surface.

UA can activate mitophagy by regulating different pathways.

A considerable number of trials have confirmed that UA has significant efficacy in improving chronic inflammation, cardiovascular diseases, muscle dysfunction, and neurodegenerative diseases.

When the model organism nematodes were fed UA for a long time (from egg stage to death), compared with the control group, UA activated their AMPK signaling pathway and significantly promoted mitophagy, extending the lifespan of the nematodes by up to 45.4%

UA significantly extends the lifespan of C. elegans in a dose-dependent manner

Urolithin A significantly improves endothelial cell survival under high glucose-induced conditions

CCK8 experimental results showed that compared with the normal control group, high glucose significantly reduced cell survival (P < 0.05), and UA (1 μmol ~ 10 μmol) increased the survival of endothelial cells in a dose-dependent manner. There was no significant difference between 10 μmol and 50 μmol (P>0.05). The UA intervention concentration in subsequent experiments was 10 μmol.

Urolithin A improves vascular endothelial dysfunction caused by high glucose environment

By detecting the secretion of NO and ET-1 by endothelial cells in each group, we evaluated the effect of UA on vascular endothelial function in a high-glucose environment. Compared with the normal control group, high sugar significantly reduced the secretion of NO (P<0.05) and increased the secretion of ET-1 (P<0.05); after adding UA (10 μmol), the secretion of NO increased significantly (P<0.05). 0.05), the secretion of ET-1 decreased (P<0.05). The regulatory effect of UA disappeared after concurrent administration of AMPK inhibitors.

Urolithin A reduces high glucose-induced oxidative stress in vascular endothelial cells

Judging from the results of DHE fluorescence staining (detection of ROS generation), fluorescence quantitative analysis and SOD activity results, compared with the normal control group, the high-glucose environment significantly increased ROS levels and decreased SOD activity in vascular endothelial cells (P<0.05); UA Incubation significantly reduced ROS levels and increased SOD activity (P<0.05); the above effects were significantly attenuated after simultaneous administration of AMPK inhibitor Compound C (P<0.05)

Urolithin A activates AMPK/eNOS pathway to improve endothelial cell damage caused by high glucose

In further exploring the mechanism, we detected the effect of UA on the AMPK/eNOS signaling pathway through Western blotting, and the corresponding protein phosphorylation levels were reflected by p-AMPK/AMPK and p-eNOS/eNOS. The results showed that compared with the normal group, the phosphorylation levels of AMPK and eNOS in endothelial cells treated with high glucose were significantly reduced (P<0.05); UA can effectively reverse the changes in phosphorylation levels of AMPK and eNOS (P<0.05); but this effect can be Antagonized by AMPK inhibitors (P<0.05). The above results indicate that UA may improve high glucose-induced endothelial cell damage by activating the AMPK/eNOS pathway.

Urolithin A has potential applications in the areas of aging, muscle health, and neurodegenerative diseases.

It has been shown to reduce the accumulation of damaged proteins in the brain and may have potential therapeutic applications in diseases such as Alzheimer's and Parkinson's.

Currently widely used in nutritional supplements, pharmaceuticals and other products

Shaanxi Yuantai Biotechnology Co., Ltd. was established in 2014, mainly supplying herbal extracts, functional cosmetic raw materials, organic products, etc. We have our own factories, R&D and quality inspection teams, and have the conditions for development, production, and quality assurance. At present, we have obtained ISO9001, ISO22000, HALAL, KOSHER, HACCP, FDA and other certificates. Therefore, the quality of our products is guaranteed, and it is our original intention to bring high-quality products to customers.

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