ODM High Quality Food Grade Health Supplement 20% Urolithin-A Liposomal Factory, Manufacturer

Better Photothermal Stability

Urolithin A

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What is S Armour Tech™Urolithin A ？

Urolithin A is obtained by fermentation and metabolism of ellagic acid by intestinal microorganisms. It is currently recognized as the raw material of mitochondrial autophagy. In today's anti-aging era, Urolithin A occupies a very important position. However, the extremely low water solubility and bioavailability of urolithin A means that we have to take a much larger amount than the actual effective amount to truly achieve the effective purpose. If we want to achieve longevity, we need to pay a higher cost to get "value for money", which is obviously unrealistic.

S Armour Tech™ Urolithin A uses ultra-high pressure homogenization technology to effectively improve the function of Urolithin A, so that the value of Urolithin A can be truly released, helping customers to make their products truly meet the needs of consumers while saving costs for customers.

20% UrolithinA Liposomal

Advantages:

Good water solubility; Good Photothermal Stability; Increase bioavailability by up to 380%

Appearance:

Light Yellow Loose Powder

Detection Method:

HPLC

Bulk Density:

0.32g/mL

100mg /20% Urolithin A Lipidosome =380 mg /20% Urolithin A

Standardized 98% Urolithin A

Advantages:

Competitive price; Advanced green technology

Graph Description:

Faint yellow powder

Detection Method:

HPLC

Bulk Density:

0.24g/mL

Functions of UrolithinA

1.Bone health

Amazentis proprietary urolithin A, also known as Mitopure, can significantly improve the mitochondrial health of healthy human knee joints and osteoarthritis knee joint chondrocytes. A mouse model of surgically induced osteoarthritis was used to test Urolithin A's ability to prevent cartilage breakdown, block inflammation, and reduce pain. After surgery, the knee develops cartilage erosion in the femur and tibia, including loss of the articular cartilage lining (superficial area). The mice were given control diet or a diet supplemented with 50 or 250 mg/kg urolixin A for 8 weeks after surgery. After 8 weeks of treatment, urolixin A significantly reduced the OARSI score (lesion severity and percentage of affected area of the entire knee joint) and circulating levels of metalloproteinase 3 (MMP3).Urolithin A prevents cartilage breakdown in a model of surgically induced osteoarthritis. Urolithin A treatment for 8 weeks after surgery induced osteoarthritis showed a protective effect on chondrocytes, reducing cartilage damage and promoting joint cell survival. Urolixin A also helps relieve the pain of osteoarthritis

2.Muscular strength, endurance and capacity

UA (500 or 1000 mg/day for 4 months) significantly increased muscle strength expressed as average peak torque in the hamstring muscle and the maximum torque during knee flexion when compared to placebo. We observe clinically meaningful improvements with Urolithin A on aerobic endurance (peak oxygen oxygen consumption [VO2]) and physical performance (6 min walk test) . Levels of plasma acylcarnitines and C-reactive proteins are significantly lower with Urolithin A, indicating higher mitochondrial efficiency and reduced inflammation. This study highlights the benefit of Urolithin A to improve muscle performance.

3.Improved Mitochondrial

Fig. 1 | UA impacts markers of mitochondrial function after 28 d of treatment

We report the results of a first-in-human clinical trial in which we administered UA, either as a single dose or as multiple doses over a 4-week period, to healthy, sedentary elderly individuals.

The direct impact of UA at the level of the skeletal muscle (vastus lateralis) was evaluated by gene expression analysis, using a series of genes related to autophagy/mitophagy, mitochondrial biogenesis and fatty acid oxidation selected on the basis of previous preclinical efficacy data1 . A general pattern of dose-dependent upregulation of gene expression in the human muscle, similar to that observed previously in preclinical models, was seen after 28 d of UA treatment at 500 and 1,000mg, with some reaching statistical significance (GABARAPL1, FABP3) (Fig. 1a). And Mitochondrial abundance was also evaluated by measuring the ratio of mitochondrial DNA to nuclear DNA (mtDNA/nuDNA) , the mtDNA/nuDNA ratio tended to increase, (Fig. 1b) .Treatment with UA at 500 and 1,000mg was seen to upregulate several mitochondrial gene sets with a false discovery rate (FDR)<0.1, including the GO_MITOCHONDRION gene set (Fig. 2c,d).

We show that UA was bioavailable in plasma at all doses tested, and 4 weeks of treatment with UA at doses of 500 mg and 1,000 mg modulated plasma acylcarnitines and skeletal muscle mitochondrial gene expression in elderly individuals (secondary outcomes). These observed effects on mitochondrial biomarkers show that UA induces a molecular signature of improved mitochondrial and cellular health following regular oral consumption in humans.

4.Antiobesity

The effect of UA on body weight: After 10 weeks of UA treatment, mice weighed 23.5% less than controls. Lower body weight in UA-treated mice resulted from the decreased fat mass (−61.3%) and a lower fat/body mass ratio (−70%).

The effects of UA on glucose metabolism: Plasma glucose concentrations (−16.2% and −29.4% after 5 and 10 weeks of treatment, respectively) and insulin (−16.7% and −37.1% after 5 and 10 weeks of treatment, respectively) were lower in UA-treated mice than those in controls.

Together, these results suggest that UA is a potent antiobesity agent with potential for human clinical applications.

5. Joint Health

In vitro, UA inhibited the interleukin-1 beta (IL-1β) induced over-production of nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in a concentration-dependent manner in human OA chondrocytes.

To investigate the mechanism of the protective effects of UA in vivo, cartilage was subjected to immunofluorescence staining to examine the nuclear translocation of p65. The cartilage of DMM mice contained chondrocytes with more red-stained nuclei . Quantitative analysis showed that treatment of DMM mice with UA significantly decreased the frequency of p65-positive nuclei . According to the X-ray shown, the DMM group showed severe narrowing of joint space and increase of cartilage surface density compared to the sham group. Nevertheless, although the narrowing of joint space exits, the calcification of cartilage surface was milder and lower narrow of joint space was observed in UA treatment group

6.Lifespan

One of the first publications to study the direct effects of UA in vivo was in the context of aging . A comparison of different pomegranate metabolites testing their impact on worm longevity showed that UA extends lifespan by 45%, while its precursor EA has no effect. After these studies in wild-type worms, the anti-aging effects of UA were also confirmed in the wrn-1 worm model of Werner syndrome, a premature aging disease . In mice, UA treatment significantly increased the survival rate of the mdx/Utr−/− double knockout (DKO) mouse model of DMD that shows premature death similar to human DMD patients.

7.Extract aged hematopoietic stem cells from aged mice (over 18 months old), treat them with urolithin A at a concentration of 20 μ M for 3 days, and then transplant them into recipient mice for myeloablative treatment. According to the research results, treatment with urolithin A can restore the hematopoietic function of aging hematopoietic stem cells to the level of young mice aged 8-12 weeks.