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Drug: Allopurinol

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Total 14 results found since Jan 2013.

Allopurinol attenuates oxidative injury in rat hearts suffered ischemia/reperfusion via suppressing the xanthine oxidase/vascular peroxidase 1 pathway
This study aims to explore whether the XO/VPO1 pathway is involved in the anti-oxidative effects of allopurinol on the myocardial I/R injury. In a rat heart model of I/R, allopurinol alleviated I/R oxidative injury accompanied by decreased XO activity, XO-derived products (H2O2 and uric acid), and VPO1 expression (mRNA and protein). In a cardiac cell model of hypoxia/reoxygenation (H/R), allopurinol or XO siRNA reduced H/R injury concomitant with decreased XO activity, VPO1 expression as well as the XO and VPO1-derived products (H2O2, uric acid, and HOCl). Although knockdown of VPO1 could also exert a beneficial effect on ...
Source: European Journal of Pharmacology - July 24, 2021 Category: Drugs & Pharmacology Authors: Yi-Shuai Zhang Li-Qun Lu Ya-Qian Jiang Nian-Sheng Li Xiu-Ju Luo Jin-Wu Peng Jun Peng Source Type: research

Allopurinol reduces oxidative stress and activates Nrf2/p62 to attenuate diabetic cardiomyopathy in rats.
Abstract Allopurinol (ALP) attenuates oxidative stress and diabetic cardiomyopathy (DCM), but the mechanism is unclear. Activation of nuclear factor erythroid 2-related factor 2 (Nrf2) following the disassociation with its repressor Keap1 under oxidative stress can maintain inner redox homeostasis and attenuate DCM with concomitant attenuation of autophagy. We postulated that ALP treatment may activate Nrf2 to mitigate autophagy over-activation and consequently attenuate DCM. Streptozotocin-induced type 1 diabetic rats were untreated or treated with ALP (100 mg/kg/d) for 4 weeks and terminated after heart functi...
Source: J Cell Mol Med - December 18, 2019 Category: Molecular Biology Authors: Luo J, Yan D, Li S, Liu S, Zeng F, Cheung CW, Liu H, Irwin MG, Huang H, Xia Z Tags: J Cell Mol Med Source Type: research

Hydralazine improves ischemia-induced neovasculogenesis via xanthine-oxidase inhibition in chronic renal insufficiency
In conclusion, hydralazine, as a potential XO inhibitor, not only reduced blood pressure and UA levels but also increased the number of circulating EPCs and improved neovasculogenesis in CRI animals. Hydralazine directly inhibited IS-induced ROS and XO activation in EPCs and endothelial cells, and restored their functions in vitro. Future studies should evaluate whether hydralazine could provide additional vascular protection in patients with CRI.Graphical abstract
Source: Pharmacological Research - November 1, 2019 Category: Drugs & Pharmacology Source Type: research

Uric Acid Induces Cardiomyocyte Apoptosis via Activation of Calpain-1 and Endoplasmic Reticulum Stress
Conclusions: These findings suggest that UA induces cardiomyocyte apoptosis through activation of calpain-1 and ER stress. These results may provide new insights into the mechanisms of hyperuricemia-associated cardiovascular risks and hopefully identify new treatment targets.Cell Physiol Biochem 2018;45:2122 –2135
Source: Cellular Physiology and Biochemistry - March 13, 2018 Category: Cytology Source Type: research

Nitrite-derived nitric oxide reduces hypoxia-inducible factor 1 α-mediated extracellular vesicle production by endothelial cells
Conclusion These data provide evidence that hypoxia enhances the release of EVs in endothelial cells, and that this is mediated by HIF-1α, but not HIF-2α. Furthermore, the reduction of NO2 − to NO via xanthine oxidoreductase during hypoxia appears to inhibit HIF-1α-mediated EV production.
Source: Nitric Oxide - December 23, 2016 Category: Chemistry Source Type: research

Hypoxanthine induces cholesterol accumulation and incites atherosclerosis in apolipoprotein E-deficient mice and cells.
In this study, we investigated the role of hypoxanthine on cholesterol synthesis and atherosclerosis development, particularly in apolipoprotein E (APOE)-deficient mice. The effect of hypoxanthine on the regulation of cholesterol synthesis and atherosclerosis were evaluated in Apoe knockout (KO) mice and cultured HepG2 cells. Hypoxanthine markedly increased serum cholesterol levels and the atherosclerotic plaque area in Apoe KO mice. In HepG2 cells, hypoxanthine increased intracellular ROS production. Hypoxanthine increased cholesterol accumulation and decreased APOE and ATP-binding cassette transporter A1 (ABCA1) mRNA and...
Source: J Cell Mol Med - July 10, 2016 Category: Molecular Biology Authors: Ryu HM, Kim YJ, Oh EJ, Oh SH, Choi JY, Cho JH, Kim CD, Park SH, Kim YL Tags: J Cell Mol Med Source Type: research

Hypoxanthine induces cholesterol accumulation and incites atherosclerosis in apolipoprotein E ‐deficient mice and cells
In this study, we investigated the role of hypoxanthine on cholesterol synthesis and atherosclerosis development, particularly in apolipoprotein E (APOE)‐deficient mice. The effect of hypoxanthine on the regulation of cholesterol synthesis and atherosclerosis were evaluated in Apoe knockout (KO) mice and cultured HepG2 cells. Hypoxanthine markedly increased serum cholesterol levels and the atherosclerotic plaque area in Apoe KO mice. In HepG2 cells, hypoxanthine increased intracellular ROS production. Hypoxanthine increased cholesterol accumulation and decreased APOE and ATP‐binding cassette transporter A1 (ABCA1) mRNA...
Source: Journal of Cellular and Molecular Medicine - July 10, 2016 Category: Molecular Biology Authors: Hye ‐Myung Ryu, You‐Jin Kim, Eun‐Joo Oh, Se‐Hyun Oh, Ji‐Young Choi, Jang‐Hee Cho, Chan‐Duck Kim, Sun‐Hee Park, Yong‐Lim Kim Tags: Original Article Source Type: research

Hypoxanthine induces cholesterol accumulation and incites atherosclerosis in apolipoprotein E‐deficient mice and cells
In this study, we investigated the role of hypoxanthine on cholesterol synthesis and atherosclerosis development, particularly in apolipoprotein E (APOE)‐deficient mice. The effect of hypoxanthine on the regulation of cholesterol synthesis and atherosclerosis were evaluated in Apoe knockout (KO) mice and cultured HepG2 cells. Hypoxanthine markedly increased serum cholesterol levels and the atherosclerotic plaque area in Apoe KO mice. In HepG2 cells, hypoxanthine increased intracellular ROS production. Hypoxanthine increased cholesterol accumulation and decreased APOE and ATP‐binding cassette transporter A1 (ABCA1) mRNA...
Source: Journal of Cellular and Molecular Medicine - July 10, 2016 Category: Molecular Biology Authors: Hye‐Myung Ryu, You‐Jin Kim, Eun‐Joo Oh, Se‐Hyun Oh, Ji‐Young Choi, Jang‐Hee Cho, Chan‐Duck Kim, Sun‐Hee Park, Yong‐Lim Kim Tags: Original Article Source Type: research

Allopurinol-induced Sweet's syndrome.
We describe the case of an 87-year-old woman with hyperuricemia who developed classic Sweet's syndrome manifestations 8 days after being treated with allopurinol. Patient's symptoms included fever, painful edema in the hands and lower limbs with non-pruritic erythematous plaques topped by pus-filled skin blisters, right eye conjunctivitis, splenomegaly and joint pain. At the emergency department, blood tests showed neutrophilic leukocytosis, inflammatory state and altered liver function. During hospitalization, she received unsuccessful treatments with two different antibiotics (namely ceftriaxone and levofloxacin), while ...
Source: International Journal of Immunopathology and Pharmacology - December 20, 2015 Category: Allergy & Immunology Tags: Int J Immunopathol Pharmacol Source Type: research

HIF-1α Activation by Intermittent Hypoxia Requires NADPH Oxidase Stimulation by Xanthine Oxidase
by Jayasri Nanduri, Damodara Reddy Vaddi, Shakil A. Khan, Ning Wang, Vladislav Makarenko, Gregg L. Semenza, Nanduri R. Prabhakar Hypoxia-inducible factor 1 (HIF-1) mediates many of the systemic and cellular responses to intermittent hypoxia (IH), which is an experimental model that simulates O2 saturation profiles occurring with recurrent apnea. IH-evoked HIF-1α synthesis and stability are due to increased reactive oxygen species (ROS) generated by NADPH oxidases, especially Nox2. However, the mechanisms by which IH activates Nox2 are not known. We recently reported that IH activates xanthine oxidase (XO) and the resulti...
Source: PLoS One - March 9, 2015 Category: Biomedical Science Authors: Jayasri Nanduri et al. Source Type: research

Pterostilbene and allopurinol reduce fructose-induced podocyte oxidative stress and inflammation via microRNA-377.
Abstract High dietary fructose is an important causative factor in the development of metabolic syndrome-associated glomerular podocyte oxidative stress and injury. Here, we identified microRNA-377 (miR-377) as a biomarker of oxidative stress in renal cortex of fructose-fed rats, which correlated with podocyte injury and albuminuria in metabolic syndrome. Fructose feeding increased miR-377 expression and decreased superoxide dismutase (SOD) expression and activity, caused O2(•-) and H2O2 over-production in kidney cortex or glomeruli of rats. This ROS induction increased p38 MAPK phosphorylation and thioredoxin-i...
Source: Free Radical Biology and Medicine - March 4, 2015 Category: Biology Authors: Wang W, Ding XQ, Gu TT, Song L, Li JM, Xue QC, Kong LD Tags: Free Radic Biol Med Source Type: research

Quercetin and allopurinol reduce liver thioredoxin‐interacting protein to alleviate inflammation and lipid accumulation in diabetic rats
Conclusions and ImplicationsInhibition of hepatic TXNIP by quercetin and allopurinol contributes to the reduction in liver inflammation and lipid accumulation under hyperglycaemic conditions. The targeting of hepatic TXNIP by quercetin and allopurinol may have therapeutic implications for prevention of type 1 diabetes‐associated NAFLD.
Source: British Journal of Pharmacology - June 21, 2013 Category: Drugs & Pharmacology Authors: Wei Wang, Chuang Wang, Xiao‐Qin Ding, Ying Pan, Ting‐Ting Gu, Ming‐Xing Wang, Yang‐Liu Liu, Fu‐Meng Wang, Shui‐Juan Wang, Ling‐Dong Kong Tags: Research Paper Source Type: research

Quercetin and Allopurinol Reduce Liver Thioredoxin‐Interacting Protein to Improve Inflammation and Lipid Accumulation in Diabetic Rats
Conclusions and ImplicationsThese results demonstrate that hepatic TXNIP inhibition by quercetin and allopurinol contributes to the improvement of liver inflammation and lipid accumulation under hyperglycemia condition. Therefore, quercetin and allopurinol targeting hepatic TXNIP may have therapeutic application to prevent type 1 diabetes‐associated NAFLD.
Source: British Journal of Pharmacology - May 3, 2013 Category: Drugs & Pharmacology Authors: Wei Wang, Chuang Wang, Xiao‐Qin Ding, Ying Pan, Ting‐Ting Gu, Ming‐Xing Wang, Yang‐Liu Liu, Fu‐Meng Wang, Shui‐Juan Wang, Ling‐Dong Kong Tags: Research Paper Source Type: research