Hydrogen Sulphide Treatment Prevents Renal Ischemia-Reperfusion Injury by Inhibiting the Expression of ICAM-1 and NF-kB Concentration in Normotensive and Hypertensive Rats

Abstract

Our main objective was to investigate the effect of chronic administration of hydrogen sulphide donor (sodium hydrosulphide) on the expression of intercellular adhesion molecule-1 (ICAM-1) and concentration of nuclear factor-kappa B (NF-kB) in a renal ischemia-reperfusion injury (IRI) model of WKY and L-nitro-arginine-methyl-ester (L-NAME)-induced hypertensive rats. Sodium hydrosulphide (NaHS) was administered intraperitoneally (i.p.) for 35 days while cystathionine gamma lyase (CSE) inhibitor dL-propargylglycine (PAG) was administered at a single dose of 50 mg/kg. Animals were anesthetised using sodium pentobarbitone (60 mg/kg) and then prepared to induce renal ischemia by clamping the left renal artery for 30 min followed by 3 h of reperfusion. Pre-treatment with NaHS improved the renal functional parameters in both WKY and L-NAME-induced hypertensive rats along with reduction of blood pressure in hypertensive groups. Oxidative stress markers like malondialdehyde (MDA), total superoxide dismutase (T-SOD) and glutathione (GSH) were also improved by NaHS treatment following renal IRI. Levels of ICAM-1 and NF-kB concentration were reduced by chronic treatment with NaHS and increased by PAG administration after renal IRI in plasma and kidney. Treatment with NaHS improved tubular morphology and glomerulus hypertrophy. Pre-treatment with NaHS reduced the degree of renal IRI by potentiating its antioxidant and anti-inflammatory mechanism, as evidenced by decreased NF-kB concentration and downregulation of ICAM-1 expression.

Pre-Treatment of Transplant Donors with Hydrogen Sulfide to Protect against Warm and Cold Ischemia-Reperfusion Injury in Kidney and Other Transplantable Solid Organs

“…This renal protection resulted in improved renal function (as measured by serum creatinine) compared to mice that received gaseous H 2 S beginning immediately before reperfusion and the control group [ 61 ]. This protective effect of H 2 S can be attributed to the induction of hypometabolism [ 61 ] as well as the suppression of oxidative stress, reduced intracellular adhesion molecule 1 (ICAM-1) expression, and increased Nrf2 nuclear translocation [ 62 , 63 , 64 ]. The protective effects of H 2 S against warm renal IRI observed in this study cannot be attributed to pretreatment alone due to the continuation of H 2 S inhalation into the ischemic period.…”

Роль Системи Гідроген Сульфіду В Механізмах Нефропротекторної Дії Метформіну За Стрептозотоциніндукованого Діабету

“…Виникає питання щодо молекулярних мішеней, через які може опосередковуватись стимулюючий вплив NaHS на нефропротекторні властивості метформіну за ЦД. Так, протизапальна активність в нирках асоціюється зі зменшенням експресії ядерного фактора NF-κB, блокуванням мітогенактивованого протеїнкіназного (МАРК) сигналінгу, що веде до зниження продукції прозапальних цитокінів [6,11]. Антифіброгенний потенціал гідроген сульфіду опосередковується через зниження активності ренін-ангіотензин-альдостеронової системи, блокування сигнальних шляхів, залежних від МАРК та трансформуючого фактора росту (TGF-β), які стимулюють процеси ремоделювання сполучної тканини [9,21].…”

Sevoflurane participates in the protection of rat renal ischemia‐reperfusion injury by down‐regulating the expression of TRPM7

“…At present, there is no effective treatment strategy to cause renal ischemia‐reperfusion injury, which mainly includes energy metabolism disorders, calcium overload, mitochondrial damage, oxidative stress, inflammation, apoptosis, and necrosis. 3 , 4 , 5 Therefore, in‐depth understandings of the mechanism of RIRI and improvement or reversal of its damage are important issues that need to be solved clinically.…”

“…Renal ischemia‐reperfusion injury is common in patients with cardiovascular surgery, trauma, shock and renal transplantation, and is the most common cause of acute kidney injury in clinical practice. At present, there is no effective treatment strategy to cause renal ischemia‐reperfusion injury, which mainly includes energy metabolism disorders, calcium overload, mitochondrial damage, oxidative stress, inflammation, apoptosis, and necrosis 3–5 . Therefore, in‐depth understandings of the mechanism of RIRI and improvement or reversal of its damage are important issues that need to be solved clinically.…”