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Drug: Acetylcysteine

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Total 43 results found since Jan 2013.

Acrolein is involved in ischemic stroke-induced neurotoxicity through spermidine/spermine-N1-acetyltransferase activation.
CONCLUSION: Overall, our current results demonstrate that acrolein is a culprit of neuronal damage through GSH depletion in stroke patients. The mechanism underlying the role of acrolein in stroke-related neuronal damage occurs through SSAT-induced polyamine oxidation by NF-kB pathway activation. These results provide a novel mechanism of neurotoxicity in stroke patients, aid in the development of neutralizing or preventive measures, and further our understanding of neural protection. PMID: 31629858 [PubMed - as supplied by publisher]
Source: Experimental Neurology - October 16, 2019 Category: Neurology Authors: Liu JH, Wang TW, Lin YY, Ho WC, Tsai HC, Chen SP, Lin AM, Liu TY, Wang HT Tags: Exp Neurol Source Type: research

Hypoxia-inducible factor 1 contributes to N-acetylcysteine's protection in stroke.
Abstract Stroke is a leading cause of adult morbidity and mortality with very limited treatment options. Evidence from pre-clinical models of ischemic stroke has demonstrated that the antioxidant N-acetylcysteine (NAC) effectively protects the brain from ischemic injury. Here, we evaluated a new pathway through which NAC exerted its neuroprotection in a transient cerebral ischemia animal model. Our results demonstrated that pre-treatment of NAC increased protein levels of hypoxia-inducible factor-1α (HIF-1α), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (...
Source: Free Radical Biology and Medicine - November 29, 2013 Category: Biology Authors: Zhang Z, Yan J, Taheri S, Liu J, Shi H Tags: Free Radic Biol Med Source Type: research

Ischemic stroke disrupts the endothelial glycocalyx through activation of proHPSE via acrolein exposure Molecular Bases of Disease
In this study, glycosaminoglycans, a component of the endothelial glycocalyx, were studied in the context of ischemic stroke using a photochemically induced thrombosis mouse model. Decreased levels of heparan sulfate and chondroitin sulfate and increased activity of hyaluronidase 1 and heparanase (HPSE) were observed in ischemic brain tissues. HPSE expression in cerebral vessels increased after stroke onset and infarct volume greatly decreased after co-administration of N-acetylcysteine + glycosaminoglycan oligosaccharides as compared with N-acetylcysteine administration alone. These results suggest that the endothelial gl...
Source: Journal of Biological Chemistry - December 25, 2020 Category: Chemistry Authors: Kenta Ko, Takehiro Suzuki, Ryota Ishikawa, Natsuko Hattori, Risako Ito, Kenta Umehara, Tomomi Furihata, Naoshi Dohmae, Robert J. Linhardt, Kazuei Igarashi, Toshihiko Toida, Kyohei Higashi Tags: Glycobiology and Extracellular Matrices Source Type: research

N ‐acetylcysteine targets 5 lipoxygenase‐derived, toxic lipids and can synergize with PGE2 to inhibit ferroptosis and improve outcomes following hemorrhagic stroke in mice
This article is protected by copyright. All rights reserved.
Source: Annals of Neurology - October 7, 2018 Category: Neurology Authors: Saravanan S. Karuppagounder, Lauren Alin, Yingxin Chen, David Brand, Megan W. Bourassa, Kristen Dietrich, Cassandra M. Wilkinson, Colby A. Nadeau, Amit Kumar, Steve Perry, John T. Pinto, Victor Darley ‐Usmar, Stephanie Sanchez, Ginger L. Mi Tags: Research Article Source Type: research

A knack for “NAC”: treatment for heat stroke induced acute liver injury: A case report
We present a case of heat stroke resulting in acute liver injury (ALI) successfully treated with intravenous N-acetylcysteine (NAC).
Source: The American Journal of Emergency Medicine - November 27, 2019 Category: Emergency Medicine Authors: Brian Monzon, Kathleen Hegarty, Megan A. Rech Source Type: research

A knack for “NAC”: Treatment for heat stroke induced acute liver injury
We present a case of heat stroke resulting in acute liver injury (ALI) successfully treated with intravenous N-acetylcysteine (NAC).
Source: The American Journal of Emergency Medicine - November 27, 2019 Category: Emergency Medicine Authors: Brian Monzon, Kathleen Hegarty, Megan A. Rech Tags: Case Report Source Type: research

The Effect of Ethyl Pyruvate and N-Acetylcysteine on Ischemia Reperfusion Injury in an Experimental Model of Ischemic Stroke
Reperfusion therapies play an important role in early-period treatment of patients presenting to the emergency department due to stroke. However, the ischemia–reperfusion injury that may occur with reperfusion must then be considered. The purpose of this study was to determine the effectiveness of N-acetylcysteine (NAC) and ethyl pyruvate in preventing ischemia–reperfusion injury.
Source: The American Journal of Emergency Medicine - June 4, 2016 Category: Emergency Medicine Authors: Turkmen Suha, Cekic Gonenc Ozgen, Karaca Yunus, Mentese Ahmet, Demir Selim, Beyhun Ercument, Sahin Aynur, Gunduz Abdulkadir, Yulug Esin, Turedi Suleyman Source Type: research

The effect of ethyl pyruvate and N-acetylcysteine on ischemia-reperfusion injury in an experimental model of ischemic stroke
Reperfusion therapies play an important role in early-period treatment for patients presenting to the emergency department due to stroke. However, the ischemia-reperfusion injury that may occur with reperfusion must then be considered. The purpose of this study was to determine the effectiveness of N-acetylcysteine (NAC) and ethyl pyruvate in preventing ischemia-reperfusion injury.
Source: The American Journal of Emergency Medicine - June 4, 2016 Category: Emergency Medicine Authors: Suha Turkmen, Ozgen Cekic Gonenc, Yunus Karaca, Ahmet Mentese, Selim Demir, Ercument Beyhun, Aynur Sahin, Abdulkadir Gunduz, Esin Yulug, Suleyman Turedi Source Type: research

Protective Effects of Brain Infarction by N-Acetylcysteine Derivatives Basic Sciences
Conclusions—The results indicate that detoxification of acrolein by NAC derivatives is caused through glutathione conjugation with acrolein catalyzed by glutathione S-transferases, which can be stabilized by NAC derivatives. This is a new concept of acrolein detoxification by NAC derivatives.
Source: Stroke - June 25, 2018 Category: Neurology Authors: Takeshi Uemura, Kenta Watanabe, Kenta Ko, Kyohei Higashi, Noriyuki Kogure, Mariko Kitajima, Hiromitsu Takayama, Koichi Takao, Yoshiaki Sugita, Akihiko Sakamoto, Yusuke Terui, Toshihiko Toida, Keiko Kashiwagi, Kazuei Igarashi Tags: Animal Models of Human Disease, Ischemia, Oxidant Stress, Ischemic Stroke Original Contributions Source Type: research

Assessing acrolein for determination of the severity of brain stroke, dementia, renal failure, and Sj ögren's syndrome.
Assessing acrolein for determination of the severity of brain stroke, dementia, renal failure, and Sjögren's syndrome. Amino Acids. 2019 Mar 12;: Authors: Igarashi K, Uemura T, Kashiwagi K Abstract It was found recently that acrolein (CH2=CH-CHO), mainly produced from spermine, is more toxic than ROS (reactive oxygen species, O 2 -· , H2O2, and ·OH). In this review, we describe how the seriousness of brain infarction, dementia, renal failure, and Sjӧgren's syndrome is correlated with acrolein. In brain infarction and dementia, it was possible to identify incipient patients with high sensitivity an...
Source: Amino Acids - March 11, 2019 Category: Biochemistry Authors: Igarashi K, Uemura T, Kashiwagi K Tags: Amino Acids Source Type: research

Preventing necroptosis by scavenging ROS production alleviates heat stress-induced intestinal injury.
Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo. These findings provide a clear target for future mechanism-based therapeutic strategies for patients diagnosed with heat stroke. PMID: 32423248 [PubMed - in process]
Source: International Journal of Hyperthermia - May 21, 2020 Category: Internal Medicine Tags: Int J Hyperthermia Source Type: research

Heat stress induces intestinal injury through lysosome- and mitochondria-dependent pathway in vivo and in vitro.
Authors: Yi G, Li L, Luo M, He X, Zou Z, Gu Z, Su L Abstract Damage to the small intestine secondary to heat stroke is a major factor in heat stroke-related morbidity and mortality. However, the underlying mechanisms by which heat stroke causes small intestinal lesions and dysfunction remain unclear. To explore the pathogenesis of small intestinal tissue and epithelial cell injury, the SW480 cell heat stress model and the mice heat stroke model were established to mimic heat stroke. Morphologic changes in intestinal tissue and increased TUNEL-positive index were induced by heat stress in vivo. Heat stress activated...
Source: Oncotarget - April 6, 2017 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

The protection conferred against ischemia-reperfusion injury in the diabetic brain by N-acetylcysteine is associated with decreased dicarbonyl stress.
Abstract Diabetes, a risk factor for stroke, leads to elevated blood methylglyoxal (MG) levels. This is due to increased MG generation from the high glucose levels, and because diabetes impairs the glutathione (GSH)-glyoxalase system for MG elimination. MG glycates proteins and causes dicarbonyl stress. We investigated the contribution of MG and GSH to stroke outcome. Cerebral ischemia/reperfusion was performed in chemical-induced (streptozotocin) and genetic Akita mouse models of Type 1 diabetes. Brain infarction and functions of the GSH-dependent MG elimination pathway were determined. Diabetes increased post-is...
Source: Free Radical Biology and Medicine - April 11, 2016 Category: Biology Authors: Wang B, Yee Aw T, Stokes KY Tags: Free Radic Biol Med Source Type: research

Potent Thrombolytic Effect of N-Acetylcysteine on Arterial Thrombi.
Conclusions -We provide evidence that NAC is an effective and safe alternative to currently available antithrombotic agents to restore vessel patency after arterial occlusion. PMID: 28487393 [PubMed - as supplied by publisher]
Source: Circulation - May 9, 2017 Category: Cardiology Authors: Martinez de Lizarrondo S, Gakuba C, Herbig BA, Repessé Y, Ali C, Denis CV, Lenting P, Touzé E, Diamond SL, Vivien D, Gauberti M Tags: Circulation Source Type: research