CAS 1143-70-0 Urolithin A - Analytical Products / Alfa Chemistry

CAT	AP1143700
CAS	1143-70-0
Structure
MDL Number	MFCD20275235
Molecular Weight	228.20

Description	≥97% (HPLC)
Solubility	DMSO: 20 mg/mL, clear
Assay	≥97% (HPLC)
Color	white to beige
Form	powder
Size	5MG, 25MG
Storage Conditions	2-8°C

Protective Effect of Urolithin a on Cisplatin-Induced Nephrotoxicity in Mice via Modulation of Inflammation and Oxidative Stress

Taile Jing, Jiezhi Liao, Kezhen Shen, Xiaoyi Chen, Zhijie Xu, Wenjun Tian, Yimin Wang, Baiye Jin, Hao Pan

Food Chem Toxicol. 2019 Jul;129:108-114.

PMID: 31014901

Tissue Deconjugation of Urolithin A Glucuronide to Free Urolithin A in Systemic Inflammation

M A Ávila-Gálvez, J A Giménez-Bastida, A González-Sarrías, J C Espín

Food Funct. 2019 Jun 19;10(6):3135-3141.

PMID: 31041969

Urolithin A Attenuates Memory Impairment and Neuroinflammation in APP/PS1 Mice

Zhuo Gong, Jingyi Huang, Biao Xu, Zhenri Ou, Le Zhang, Xiaohong Lin, Xiujuan Ye, Xuejian Kong, Dahong Long, Xiangdong Sun, Xiaosong He, Liping Xu, Qingqing Li, Aiguo Xuan

J Neuroinflammation. 2019 Mar 14;16(1):62.

PMID: 30871577

Urolithin A Induces Mitophagy and Prolongs Lifespan in C. Elegans and Increases Muscle Function in Rodents

Dongryeol Ryu, Laurent Mouchiroud, Pénélope A Andreux, Elena Katsyuba, Norman Moullan, Amandine A Nicolet-Dit-Félix, Evan G Williams, Pooja Jha, Giuseppe Lo Sasso, Damien Huzard, Patrick Aebischer, Carmen Sandi, etc.

Nat Med. 2016 Aug;22(8):879-88.

PMID: 27400265

Urolithin A-activated Autophagy but Not Mitophagy Protects Against Ischemic Neuronal Injury by Inhibiting ER Stress in Vitro and in Vivo

Anil Ahsan, Yan-Rong Zheng, Xiao-Li Wu, Wei-Dong Tang, Meng-Ru Liu, Shi-Jia Ma, Lei Jiang, Wei-Wei Hu, Xiang-Nan Zhang, Zhong Chen

CNS Neurosci Ther. 2019 Sep;25(9):976-986.

PMID: 30972969

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Case Study

Urolithin A Prevents Acetaminophen-Induced Liver Injury in Mice

Gao, Zhimin, et al. International journal of biological sciences 18.5 (2022): 2146.

Acetaminophen overdose is a leading cause of acute liver failure worldwide. N-acetylcysteine (NAC), the only available antidote, has limitations due to its narrow therapeutic time window. Here, we demonstrate that Urolithin A (UA), a metabolite of tannin natural products from the gastrointestinal microbiota, can prevent acetaminophen-induced liver injury (AILI) and is superior to NAC in terms of dosage and therapeutic time window.
Transcriptomic analysis shows that UA promotes mitochondrial autophagy in the liver and activates the Nrf2/ARE signaling pathway. Consistent with this, less oxidative stress was observed in the liver treated with UA due to the activation of mitochondrial autophagy and the Nrf2/ARE signaling pathway. Subsequent molecular docking and dynamics simulations revealed the binding patterns of UA with Nrf2/Keap1, including a hydrogen bond network between the oxygen atoms in UA and residues Arg 415, Ser 508, and Ser 602 of Nrf2/Keap1, which triggers Nrf2 nuclear translocation and subsequently activates Nrf2 target genes (HO-1, NQO1). Notably, inhibition of mitochondrial autophagy did not prevent UA's protective effects against AILI; instead, it was compromised by both in vivo and in vitro Nrf2 gene silencing.
In summary, our data indicate that UA alleviates acetaminophen-induced oxidative stress and liver necrosis by activating the Nrf2/ARE signaling pathway, highlighting its therapeutic potential for AILI.

Urolithin A Protects Pancreatic β Cells from Apoptosis by Activating Autophagy

Zhang, YanZhi, et al. Journal of Ethnopharmacology 272 (2021): 113628.

Urolithin A is an active metabolite of the plant polyphenol ellagic acid produced by gut microbiota, derived from strawberries and traditional anti-diabetic herbs such as pomegranate and emblic. This study aimed to investigate whether Urolithin A can protect pancreatic β cells from apoptosis induced by glucolipotoxicity and its potential mechanisms.
Glucolipotoxicity leads to mitochondrial damage (decreased mitochondrial membrane potential ΔΨm and cleavage of caspase-3) and autophagy defects, resulting in β cell apoptosis in type 2 diabetes. Urolithin A intervention significantly reduced pancreatic cell apoptosis in diabetic mice and MIN6 β cells. This effect was achieved by downregulating cleaved-caspase-3 and cleaved-caspase-1, as well as restoring cell viability, cell morphology, and mitochondrial membrane potential, alongside the downregulation of the autophagy protein SQSTM1/p62 and the upregulation of LC3II.

Mechanism of Urolithin A's Action on High-Glucose-Induced Neuronal Amyloidosis

Lee, Hyun Jik, et al. Cell Death & Differentiation 28.1 (2021): 184-202.

Urolithin A, a novel candidate drug with antioxidant and neuroprotective effects, has been receiving increasing attention in the context of Alzheimer's disease (AD).
In this study, we investigated the effects of Urolithin A on high-glucose-induced amyloidosis, which is caused by mitochondrial calcium dysregulation and mtROS accumulation, leading to neuronal degeneration. The mechanisms associated with the formation of mitochondrial-associated endoplasmic reticulum membranes (MAM) were also identified.
We found that Urolithin A significantly reduced mitochondrial calcium influx, alleviating high-glucose-induced mtROS accumulation and the expression of amyloid precursor protein (APP) and β-secretase-1 (BACE1), the enzymes responsible for amyloid beta (Aβ) production. In a streptozotocin (STZ)-induced diabetic mouse model, the injection of Urolithin A reduced APP and BACE1 expression, Tau phosphorylation, Aβ deposition, and cognitive impairment.
Furthermore, high glucose stimulated MAM formation and the expression of transglutaminase 2 (TGM2). This study first demonstrated that Urolithin A significantly decreased high-glucose-induced TGM2 expression. Notably, the disruption of the AIP-AhR complex was associated with the inhibition of high-glucose-induced TGM2 expression mediated by Urolithin A. Silencing TGM2 was found to inhibit the interaction between inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) and voltage-dependent anion channel protein 1 (VDAC1), thus preventing high-glucose-induced mitochondrial calcium influx and mtROS accumulation.
We also discovered that either Urolithin A or TGM2 silencing could prevent Aβ-induced mitochondrial calcium influx, mtROS accumulation, Tau phosphorylation, and cell death in neuronal cells.