Sodium thiosulfate protects brain in rat model of adenine induced vascular calcification

Subhash, N.; Sriram, R.; Kurian, Gino A.

doi:10.1016/j.neuint.2015.09.004

Cited by 28 publications

(15 citation statements)

References 28 publications

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“…In the present study, we found aortic calcifications in Adenine group. These results are in line with previous studies (Subhash et al 2015;Ravindran et al 2017aRavindran et al , 2017b. VC are not passive process, but it is an active process, in which the vascular cells are transformed to osteoblast like cells.…”

Section: Discussionsupporting

confidence: 93%

Effects of nicorandil on vascular and renal dysfunctions in adenine-induced nephropathy: Possible underlying mechanisms

Hussein

El-Dosoky²,

Malek³

et al. 2019

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Vascular dysfunctions in chronic kidney disease (CKD) include endothelial dysfunctions and vascular calcification (VC). In the present study, we examined the possible protective effect of nicorandil (potassium channel opener) on renal and vascular dysfunctions in a rat model of adenine-induced nephropathy and its underlying mechanisms. Thirty-four male Sprague-Dawley rats were randomly allocated into 3 groups: Control group, Adenine group (animals received high-adenine diet for 4 weeks), and Nicorandil group (animals received adenine for 4 weeks and nicorandil 1 mg/kg per oral for 4 weeks). The results showed significant reduction in the body weight, heart rate (HR), hemoglobin contents, serum Ca 2+ and reduction in the expression of mRNA of endothelial nitric oxide synthase (eNOS) and nuclear factor erythroid related factor 2 (nrf2) genes in aortic tissues with significant increase in arterial blood pressure (ABP), serum creatinine, blood urea nitrogen (BUN), plasma renin activity (PRA), K + and phosphate (PO 4 3-), urinary albumin excretion (UAE) and aortic VC in Adenine group compared to normal group (p < 0.05). On the other hand, coadminsitration of nicorandil caused significant improvement in the studied parameters compared to Adenine group (p < 0.05). We concluded that nicorandil has a potential protective effect against the vascular and renal impairment induced by adenine, which might be due to attenuation of vascular calcifications, activation of Nrf2 and eNOS genes in aortic tissues.

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Section: Discussionsupporting

confidence: 93%

Effects of nicorandil on vascular and renal dysfunctions in adenine-induced nephropathy: Possible underlying mechanisms

Hussein

El-Dosoky²,

Malek³

et al. 2019

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“…In vivo and in vitro experiments both indicate that H 2 S inhibits the phenotype transformation of VSMCs and alleviates VC [ 9 ]. In the present experiment, the calcium content of the aorta and ALP activity of the VDN group were both higher compared with that of the control group, while NaHS treatment significantly alleviated such increase.…”

Section: Discussionmentioning

confidence: 99%

“…H 2 S affects the cardiovascular system in multiple ways, by dilating blood vessels, lowering blood pressure [ 8 ], and regulating the apoptosis and proliferation of VSMCs. Recent studies have suggested that H 2 S also inhibits VC and the phenotype transformation of VSMCs [ 9 ]. However, the specific mechanism is unknown.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Improves Vascular Calcification in Rats by Inhibiting Endoplasmic Reticulum Stress

Yang

Teng

et al. 2016

Oxidative Medicine and Cellular Longevity

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In this study, the vitamin D3 plus nicotine (VDN) model of rats was used to prove that H2S alleviates vascular calcification (VC) and phenotype transformation of vascular smooth muscle cells (VSMC). Besides, H2S can also inhibit endoplasmic reticulum stress (ERS) of calcified aortic tissues. The effect of H2S on alleviating VC and phenotype transformation of VSMC can be blocked by TM, while PBA also alleviated VC and phenotype transformation of VSMC that was similar to the effect of H2S. These results suggest that H2S may alleviate rat aorta VC by inhibiting ERS, providing new target and perspective for prevention and treatment of VC.

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“…The cellular uptake of sodium thiosulfate involves the sodium sulfate cotransporter 2 (Marutani et al, 2015). In vivo, its therapeutic efficacy in rodent models of LPS-induced lung injury (Sakaguchi et al, 2014), galactosamine/LPS-induced acute liver failure (Shirozu et al, 2014), angiotensin-induced hypertension and hypertensive heart disease (Snijder et al, 2014;Snijder et al, 2015), global cerebral ischemia (Marutani et al, 2015), vascular calcification (Subhash et al, 2015), and hyperoxaluric renal dysfunction (Bijarnia et al, 2015) can be seen at doses ranging from 10 to 2000 (mg/kg)/day. In clinical observational studies, plasma thiosulfate levels show positive correlations, with improved clinical outcomes in renal transplantation Frenay et al, 2016).…”

Section: Alternative Means To Increase Biologic H 2 S Levelsmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H₂S Levels: H₂S Donors and H₂S Biosynthesis Inhibitors

2017

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Over the last decade, hydrogen sulfide (HS) has emerged as an important endogenous gasotransmitter in mammalian cells and tissues. Similar to the previously characterized gasotransmitters nitric oxide and carbon monoxide, HS is produced by various enzymatic reactions and regulates a host of physiologic and pathophysiological processes in various cells and tissues. HS levels are decreased in a number of conditions (e.g., diabetes mellitus, ischemia, and aging) and are increased in other states (e.g., inflammation, critical illness, and cancer). Over the last decades, multiple approaches have been identified for the therapeutic exploitation of HS, either based on HS donation or inhibition of HS biosynthesis. HS donation can be achieved through the inhalation of HS gas and/or the parenteral or enteral administration of so-called fast-releasing HS donors (salts of HS such as NaHS and NaS) or slow-releasing HS donors (GYY4137 being the prototypical compound used in hundreds of studies in vitro and in vivo). Recent work also identifies various donors with regulated HS release profiles, including oxidant-triggered donors, pH-dependent donors, esterase-activated donors, and organelle-targeted (e.g., mitochondrial) compounds. There are also approaches where existing, clinically approved drugs of various classes (e.g., nonsteroidal anti-inflammatories) are coupled with HS-donating groups (the most advanced compound in clinical trials is ATB-346, an HS-donating derivative of the non-steroidal anti-inflammatory compound naproxen). For pharmacological inhibition of HS synthesis, there are now several small molecule compounds targeting each of the three HS-producing enzymes cystathionine--synthase (CBS), cystathionine--lyase, and 3-mercaptopyruvate sulfurtransferase. Although many of these compounds have their limitations (potency, selectivity), these molecules, especially in combination with genetic approaches, can be instrumental for the delineation of the biologic processes involving endogenous HS production. Moreover, some of these compounds (e.g., cell-permeable prodrugs of the CBS inhibitor aminooxyacetate, or benserazide, a potentially repurposable CBS inhibitor) may serve as starting points for future clinical translation. The present article overviews the currently known HS donors and HS biosynthesis inhibitors, delineates their mode of action, and offers examples for their biologic effects and potential therapeutic utility.

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Sodium thiosulfate protects brain in rat model of adenine induced vascular calcification

Cited by 28 publications

References 28 publications

Effects of nicorandil on vascular and renal dysfunctions in adenine-induced nephropathy: Possible underlying mechanisms

Effects of nicorandil on vascular and renal dysfunctions in adenine-induced nephropathy: Possible underlying mechanisms

Hydrogen Sulfide Improves Vascular Calcification in Rats by Inhibiting Endoplasmic Reticulum Stress

International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H₂S Levels: H₂S Donors and H₂S Biosynthesis Inhibitors

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Sodium thiosulfate protects brain in rat model of adenine induced vascular calcification

Cited by 28 publications

References 28 publications

Effects of nicorandil on vascular and renal dysfunctions in adenine-induced nephropathy: Possible underlying mechanisms

Effects of nicorandil on vascular and renal dysfunctions in adenine-induced nephropathy: Possible underlying mechanisms

Hydrogen Sulfide Improves Vascular Calcification in Rats by Inhibiting Endoplasmic Reticulum Stress

International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H2S Levels: H2S Donors and H2S Biosynthesis Inhibitors

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International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H₂S Levels: H₂S Donors and H₂S Biosynthesis Inhibitors