Diallyl trisulfide protects against ethanol-induced oxidative stress and apoptosis via a hydrogen sulfide-mediated mechanism

2016 ◽  
Vol 36 ◽  
pp. 23-30 ◽  
Author(s):  
Lian-Yun Chen ◽  
Qin Chen ◽  
Xiao-Jing Zhu ◽  
De-Song Kong ◽  
Li Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Diallyl Trisulfide

scholarly journals Diallyl Trisulfide Suppresses Oxidative Stress-Induced Activation of Hepatic Stellate Cells through Production of Hydrogen Sulfide

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Feng Zhang ◽  
Huanhuan Jin ◽  
Li Wu ◽  
Jiangjuan Shao ◽  
Xiaojing Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Hepatic Stellate Cells ◽  
Lipid Peroxide ◽  
Stellate Cells ◽  
Cyclin B1 ◽  
Diallyl Trisulfide ◽  
Fibrotic Liver ◽  
Production Of Hydrogen ◽  
And Oxidative Stress

Accumulating data reveal that garlic has beneficial effects against chronic liver disease. We previously reported that diallyl trisulfide (DATS), the primary organosulfur compound in garlic, reduced fibrosis and attenuated oxidative stress in rat fibrotic liver. The present study was aimed at elucidating the underlying mechanisms. The primary rat hepatic stellate cells (HSCs) were cultured and stimulated with hydrogen peroxide (H2O2) for inducing HSC activation under oxidative stress. We examined the effects of DATS on the profibrogenic properties and oxidative stress in H2O2-treated HSCs. The results showed that DATS suppressed and reduced fibrotic marker expression in HSCs. DATS arrested cell cycle at G2/M checkpoint associated with downregulating cyclin B1 and cyclin-dependent kinase 1, induced caspase-dependent apoptosis, and reduced migration in HSCs. Moreover, intracellular levels of reactive oxygen species and lipid peroxide were decreased by DATS, but intracellular levels of glutathione were increased in HSCs. Furthermore, DATS significantly elevated hydrogen sulfide (H2S) levels within HSCs, but iodoacetamide (IAM) reduced H2S levels and significantly abrogated DATS production of H2S within HSCs. IAM also abolished all the inhibitory effects of DATS on the profibrogenic properties and oxidative stress in HSCs. Altogether, we demonstrated an H2S-associated mechanism underlying DATS inhibition of profibrogenic properties and alleviation of oxidative stress in HSCs. Modulation of H2S production may represent a therapeutic remedy for liver fibrosis.

Abstract 229: Hydrogen sulfide donor, the Organic Polysulfide Diallyl Trisulfide Augments Ischemia-induced Angiogenesis by Upregulation of VEGF-Akt-eNOS Pathway

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Ryo Hayashida ◽  
Kazuhisa Kondo ◽  
Satoshi Shintani ◽  
Toyoaki Murohara
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Hydrogen Sulfide ◽  
Mrna Level ◽  
Capillary Density ◽  
Serum Starvation ◽  
Diallyl Trisulfide ◽  
Artery Ligation ◽  
Perfusion Image ◽  
And Oxidative Stress

Introduction: Hydrogen sulfide (H2S) upregulates anti-oxidant, anti-apoptosis, anti-inflammatory, and cell survival. H2S plays an extremely important role in the homeostasis of the cardiovascular system and in the pathogenesis of cardiovascular disease. The diallyl trisulfide (DATS) is a polysulfide constituent found in garlic oil, and known as H2S donor that is able to release H2S continuously. Peripheral artery disease (PAD) causes considerable morbidity and mortality. The aim of this study was investigate whether the DATS would augment ischemia-induced angiogenesis. Methods: The unilateral permanent femoral artery ligation was performed in C57BL/6J mice (8-10 weeks old, n=8-10/group) and eNOS KO mice (8-10 weeks old, n=5-8/group), and vehicle or DATS (500 μg/kg/day) was injected intra-peritonealy up to 1 week following the hind limb ischemia (HLI). We evaluated the blood flow recovery using the laser Doppler perfusion image and capillary density stained with CD31 at 3 weeks following HLI. We assessed VEGF level by qPCR analysis and activations of eNOS and Akt by western blot analysis in ischemic tissues. Moreover, we cultured HUVECs in a hypoxic chamber with serum starvation for 24 hour, and then evaluated apoptosis by tunnel staining and oxidative stress by DHE staining with or without DATS (50 μmol). We also evaluated activations of eNOS and Akt in cultured HUVECs with or without DATS. Results: DATS treatment significantly increased blood flow (0.45 vs 0.78,p<0.05) and capillary density (1.57 vs 1.85,p<0.05) at 3 weeks following HLI compared to vehicle. DATS also increased mRNA level of VEGF and activation of Akt and eNOS at 3 days following HLI. On the other hand, DATS treatment failed to increase blood flow and capillary density at 3 weeks following HLI in eNOS KO mice. The DATS treatment inhibited apoptosis and oxidative stress in cultured HUVECs via activation of Akt and eNOS pathway in vitro. Conclusions: Our results indicate that DATS treatment could augment ischemia-induced angiogenesis by upregulation of VEGF-Akt-eNOS pathway that leads to inhibitions of apoptosis and oxidative stress. These results suggest that administration of H2S releasing agents might be efficacious for the treatment of PAD.

scholarly journals The hydrogen sulfide releasing compounds ATB-346 and diallyl trisulfide attenuate streptozotocin-induced cognitive impairment, neuroinflammation, and oxidative stress in rats: involvement of asymmetric dimethylarginine

2016 ◽  
Vol 94 (7) ◽  
pp. 699-708 ◽  
Author(s):  
Dalia K. Mostafa ◽  
Nesrine M. El Azhary ◽  
Rasha A. Nasra
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Cognitive Impairment ◽  
Asymmetric Dimethylarginine ◽  
Therapeutic Potential ◽  
Memory Function ◽  
Diallyl Trisulfide ◽  
Beneficial Effects ◽  
Behavioural Performance ◽  
And Oxidative Stress

Hydrogen sulfide (H2S) has attracted interest as a gaseous mediator involved in diverse processes in the nervous system, particularly with respect to learning and memory. However, its therapeutic potential in Alzheimer disease (AD) is not fully explored. Therefore, the effects of H2S-releasing compounds against AD-like behavioural and biochemical abnormalities were investigated. Memory deficit was induced by intracerberoventicular injection of streptozotocin (STZ, 3 mg·kg−1). Animals were randomly assigned into 5 groups (12 rats each): normal control, STZ treated, and 3 drug-treated groups receiving naproxen, H2S-releasing naproxen (ATB-346), and diallyl trisulfide in 20, 32, 40 mg·kg−1·day−1, respectively. Memory function was assessed by passive avoidance and T-maze tasks. After 21 days, hippocampal IL-6, malondialdehyde, reduced glutathione (GSH), asymmetric dimethylarginine (ADMA), and acetylcholinestrase activity were determined. ATB-346 and diallyl trisulfide ameliorated behavioural performance and reduced malondialdehyde, ADMA, and acetylcholinestrase activity while increasing GSH. This study demonstrates the beneficial effects of H2S release in STZ-induced memory impairment by modulation of neuroinflammation, oxidative stress, and cholinergic function. It also delineates the implication of ADMA to the cognitive impairment induced by STZ. These findings draw the attention to H2S-releasing compounds as new candidates for treating neurodegenerative disorders that have prominent oxidative and inflammatory components such as AD.

scholarly journals Fighting Oxidative Stress with Sulfur: Hydrogen Sulfide in the Renal and Cardiovascular Systems

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 373
Author(s):  
Joshua J. Scammahorn ◽  
Isabel T. N. Nguyen ◽  
Eelke M. Bos ◽  
Harry Van Goor ◽  
Jaap A. Joles
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Redox Status ◽  
The Body ◽  
Therapeutic Interventions ◽  
Oxygen Species ◽  
Enzymatic Production ◽  
Age Related ◽  
Anti Oxidant ◽  
Enzymatic Pathways

Hydrogen sulfide (H2S) is an essential gaseous signaling molecule. Research on its role in physiological and pathophysiological processes has greatly expanded. Endogenous enzymatic production through the transsulfuration and cysteine catabolism pathways can occur in the kidneys and blood vessels. Furthermore, non-enzymatic pathways are present throughout the body. In the renal and cardiovascular system, H2S plays an important role in maintaining the redox status at safe levels by promoting scavenging of reactive oxygen species (ROS). H2S also modifies cysteine residues on key signaling molecules such as keap1/Nrf2, NFκB, and HIF-1α, thereby promoting anti-oxidant mechanisms. Depletion of H2S is implicated in many age-related and cardiorenal diseases, all having oxidative stress as a major contributor. Current research suggests potential for H2S-based therapies, however, therapeutic interventions have been limited to studies in animal models. Beyond H2S use as direct treatment, it could improve procedures such as transplantation, stem cell therapy, and the safety and efficacy of drugs including NSAIDs and ACE inhibitors. All in all, H2S is a prime subject for further research with potential for clinical use.

ACS67, a Hydrogen Sulfide–Releasing Derivative of Latanoprost Acid, Attenuates Retinal Ischemia and Oxidative Stress to RGC-5 Cells in Culture

2010 ◽  
Vol 51 (1) ◽  
pp. 284 ◽  
Author(s):  
Neville N. Osborne ◽  
Dan Ji ◽  
Aman S. Abdul Majid ◽  
Rebecca J. Fawcett ◽  
Anna Sparatore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Retinal Ischemia ◽  
Cells In Culture ◽  
And Oxidative Stress

3-Mercaptopyruvate sulfurtransferase: an enzyme at the crossroads of sulfane sulfur trafficking

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Brandán Pedre ◽  
Tobias P. Dick
Keyword(s):  
Oxidative Stress ◽  
Metabolic Disease ◽  
Hydrogen Sulfide ◽  
Fatty Acid ◽  
Stress Resistance ◽  
Respiratory Function ◽  
Acid Metabolism ◽  
Cyanide Detoxification ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Sulfur Trafficking

Abstract3-Mercaptopyruvate sulfurtransferase (MPST) catalyzes the desulfuration of 3-mercaptopyruvate to generate an enzyme-bound hydropersulfide. Subsequently, MPST transfers the persulfide’s outer sulfur atom to proteins or small molecule acceptors. MPST activity is known to be involved in hydrogen sulfide generation, tRNA thiolation, protein urmylation and cyanide detoxification. Tissue-specific changes in MPST expression correlate with ageing and the development of metabolic disease. Deletion and overexpression experiments suggest that MPST contributes to oxidative stress resistance, mitochondrial respiratory function and the regulation of fatty acid metabolism. However, the role and regulation of MPST in the larger physiological context remain to be understood.

NaHS inhibits NF-κB signal against inflammation and oxidative stress in post-infectious irritable bowel syndrome

RSC Advances ◽  
2016 ◽  
Vol 6 (69) ◽  
pp. 64208-64214 ◽  
Author(s):  
Shenglan Yang ◽  
Danfang Deng ◽  
Yingying Luo ◽  
Yanran Wu ◽  
Rui Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Irritable Bowel Syndrome ◽  
Hydrogen Sulfide ◽  
Murine Model ◽  
Irritable Bowel ◽  
And Oxidative Stress ◽  
Post Infectious

In this study, the alleviating role of hydrogen sulfide (H2S) was investigated in a Post-Infectious Irritable Bowel Syndrome (PI-IBS) murine model and Caco-2 cells.

scholarly journals A Hypothesis: Hydrogen Sulfide Might Be Neuroprotective against Subarachnoid Hemorrhage Induced Brain Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yong-Peng Yu ◽  
Xiang-Lin Chi ◽  
Li-Jun Liu
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
The Brain

Gases such as nitric oxide (NO) and carbon monoxide (CO) play important roles both in normal physiology and in disease. Recent studies have shown that hydrogen sulfide (H2S) protects neurons against oxidative stress and ischemia-reperfusion injury and attenuates lipopolysaccharides (LPS) induced neuroinflammation in microglia, exhibiting anti-inflammatory and antiapoptotic activities. The gas H2S is emerging as a novel regulator of important physiologic functions such as arterial diameter, blood flow, and leukocyte adhesion. It has been known that multiple factors, including oxidative stress, free radicals, and neuronal nitric oxide synthesis as well as abnormal inflammatory responses, are involved in the mechanism underlying the brain injury after subarachnoid hemorrhage (SAH). Based on the multiple physiologic functions of H2S, we speculate that it might be a promising, effective, and specific therapy for brain injury after SAH.

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