Sodium hydrosulphide against renal ischemia/reperfusion and the possible contribution of nitric oxide in adult male Albino rats

Abstract

OBJECTIVES: This study evaluates the effects produced by H 2 S donor; sodium hydrosulfi de (NaHS), in a renal ischemia/reperfusion (IR) rat model and assesses the possible mediating role of nitric oxide (NO) in these H 2 S' effects. BACKGROUND: For several centuries, hydrogen sulfi de (H 2 S) had been known to be a highly toxic agent. Recent studies, however, indicated that apart from NO and CO, H 2 S is the third "gasotransmitter" involved in the regulation of various physiological functions. Nevertheless, its impact on renal IR injury remains unclear. METHODS: Rats were randomly divided into three groups: sham control; renal IR; and renal IR+NaHS groups. NaHS (100 μmol/kg, ip) was administered 30 min prior to the induction of renal ischemia. RESULTS: NaHS was found to attenuate signifi cantly the IR-induced elevations in the serum levels of urea, creatinine and tumor necrosis factor α (TNF-α) as compared with IR group. NaHS also signifi cantly compensated the defi cits in the total antioxidant capacities (TAC) and lowered the elevated malondialdehyde (MDA) levels observed with renal IR in renal, hepatic, pulmonary, and cardiac tissues. Furthermore, NaHS pretreatment down-regulated the renal IR-induced over-expression of inducible nitric oxide synthase (iNOS) and up-regulated the IR-induced suppression of endothelial nitric oxide synthase (eNOS). The loss of normal architecture, hemorrhage, and infl ammatory cells infi ltration detected by histopathological examination of renal, hepatic, pulmonary, and cardiac tissues in IR rats were markedly ameliorated by pre-ischemic NaHS treatment. CONCLUSION: NaHS protects against the effects of renal IR injury by acting primarily through a decrease in both pro-infl ammatory cytokines and iNOS expression as well as through up-regulation of the eNOS pathway. Furthermore, H 2 S has a powerful anti-oxidant and anti-apoptotic effects (Tab. 2, Fig. 6, Ref. 45). Text in PDF www.elis.sk. KEY WORDS:Hydrogen sulfi de, ischemia/reperfusion injury, nitric oxide, tumor necrosis factor α, malondialdehyde, total antioxidant capacities.

Evaluation with endothelial nitric oxide synthase (eNOS) immunoreactivity of the protective role of astaxanthin on hepatorenal injury of remote organs caused by ischaemia reperfusion of the lower extremities

“…These findings are consistent with those of the above mentioned research in which different antioxidants were administered to avoid or lessen the damage caused by I/R. To inactivate the free oxygen radicals forming in the kidney I/R models, agents such as iloprost [41], sodium hydrosulphide [42], red propolis [43], menhaden oil [17], and grape seed [44] were used. Additionally, Ozkan et al [44] investigated the protective effect of grape seed proanthocyanidin in I/R damage.…”

Evaluation of combined therapeutic effects of hydrogen sulfide donor sodium hydrogen sulfide and phosphodiesterase type‐5 inhibitor tadalafil on erectile dysfunction in a partially bladder outlet obstructed rat model

“…In an experimental model of metabolic syndrome in rabbits, tadalafil reduced the gene expression of inflammation‐related markers in the bladder 18 . Furthermore, NaHS treatment downregulated the renal ischemia/reperfusion‐induced overexpression of iNOS 19 . In addition, increased MDA levels in the penis of PBOO and NaHS‐treated obstructed rats demonstrated sufficiently high levels of NF‐κB and iNOS to cause oxidative stress.…”

Evaluation of Vitamin C Supplementation on Kidney Function and Vascular Reactivity Following Renal Ischemic Injury in Mice

“…Meanwhile, enhanced vasoconstriction has been documented as a result of increased reactive oxygen species (ROS) and ROS could also impair vascular reactivity due to declining nitric oxide (NO) bioavailability [8]. It is well-known that NO participates in the pathophysiology of ARF and plays a great role in renal IRI [9][10][11][12][13][14][15]. The cross talk between ROS and NO has been well elucidated [16,17].…”