Sodium hydrogen sulfide (NaHS) ameliorates alterations caused by cisplatin in filtration slit diaphragm and podocyte cytoskeletal in rat kidney

Abstract

Background: Hydrogen sulfide (H2S) has been shown to have a protective role in various kidney disorders. Objectives: This study investigated the molecular mechanism of NaHS (a H2S donor) in treating on the renal damage induced by cisplatin (CP).Materials and Methods: Thirty-two male rats were randomly divided into 4 groups: Normal control group (group A)‚ NaHS group (group B) which received 200 µg/kg/d (intraperitoneal injection; i.p.) for 15 days‚ CP group (group C) which rats were injected with CP (5 mg/kg, single dose, i.p.), and CP + NaHS group (group D) (5 mg/kg and 200 µg/kg, respectively, i.p.). Samples of urine and serum, tissue of kidney were collected for analysis after treatments for 15 days. Morphological changes were elevated under light microscope‚ protein expression of desmin and nephrin were determined by immunohistochemistry and western blotting and also malondialdehyde (MDA) level was determined by spectrophotometer. Results: Compared to the CP group, NaHS treatment mitigated histological damages, decreased 24-hour urine protein excretion, serum urea and creatinine as well as MDA level. NaHS treatment increased protein levels of nephrin. Moreover, NaHS treatment decreased protein levels of desmin. Conclusions: NaHS can ameliorate CP -induced renal damage in rats which is associated with the increase in nephrin protein expression, and the decrease in MDA level and desmin protein expression.

Pseudoginsengenin DQ Exhibits Therapeutic Effects in Cisplatin-Induced Acute Kidney Injury via Sirt1/NF-κB and Caspase Signaling Pathway without Compromising Its Antitumor Activity in Mice

“…Apoptosis is an important factor in the pathogenesis of CDDP-induced AKI [ 6 , 7 ]. Under normal circumstances, apoptosis is a permanent and fundamental form of programmed cell death that occurs in multicellular organisms [ 8 ].…”

Polysulfide and Hydrogen Sulfide Ameliorate Cisplatin-Induced Nephrotoxicity and Renal Inflammation through Persulfidating STAT3 and IKKβ

“…Moreover, Liu and colleagues used GYY4137 at a low dose of GYY4137 (21 mg/kg) in mice, and it is highly probable that H 2 S might be insufficiently provided at lower concentrations considering the H 2 S release characteristics of GYY4137 [ 51 , 52 , 53 ]. On these grounds, a commonly used dose of GYY4137 (100 mg/kg; dissolved in PBS) was prepared in our animal studies, and GYY4137 largely ameliorated cisplatin-induced renal dysfunction and damage, which is in-keeping with the results of NaHS (another H 2 S donor) application in animals [ 54 , 55 , 56 ]. These results clearly demonstrated the protective actions of H 2 S donors against cisplatin-induced nephrotoxicity.…”

Roles of Hydrogen Sulfide Donors in Common Kidney Diseases

“…Alternatively, it has been reported that treatment with GYY4137 and NaHS exert antitoxicity effects through the reduction of ROS and the inhibition of nicotinamide adenine dinucleotide phosphate and MAPK activities in cisplatinadministered porcine renal proximal tubule cell line LLC-PK1 . NaHS can also upregulate the expression of nephrin and reduce the level of desmin (Karimi and Absalan, 2017). In addition, treatment with diallyl disulfide (DADS) alleviates nephrotoxic effects of cisplatin by increasing antioxidant defense and suppressing apoptotic, oxidative, and inflammatory activities (Elkhoely and Kamel, 2018).…”

“…Kidney works together with the renin-angiotensin-aldosterone system (RAAS) to regulate BP and maintain electrolyte balance ( Cortinovis et al, 2016 ). The decline in BP and Na + level or the stimulation of β1-adrenoreceptors can result in the secretion of renin, which in turn converts angiotensinogen (produced in the liver) into angiotensin-I which is then converted to angiotensin II by angiotensin-I converting enzyme (ACE) ( Soubrier et al, 1993 ; Deschepper, 1994 ). Angiotensin II acts on several receptors to mediate the downstream effects.…”