Ameliorated and antioxidant effects of Fucoidan against cyclosporine A-induced kidney injury in rats

Abstract

Background: Cyclosporine A (CsA) is an immunosuppression agent used frequently in fields of organs transplantation and autoimmune diseases. However, CsA-induced kidney injury is a major clinical problem associated with CsA therapy in which the conceivable accountable mechanism is oxidative stress (OS). The present study evaluated the protective and ameliorated effects of fucoidan (FU) as an antioxidant and an anti-inflammatory agent against CsA-induced kidney injury. Methods: Male rats were randomly divided into three groups. The first group was served as a control group that administered olive oil orally and normal saline subcutaneously, the second group (CA) was treated with CsA orally, and the third group (CA + FU) was treated with CsA orally in concomitant with FU subcutaneously. Experimental animals were sacrificed 20 days following the treatment period and serum samples were analyzed for creatinine test. The homogenate of renal tissues was prepared for OS assessment. Light and ultrastructure microscopic kidney sections were prepared for histopathological examination. Results: Treatment of rats with CsA alone produced a significant increase in the levels of creatinine, nitric oxide (NO), and malondialdehyde (MDA), as well as the activities of superoxide dismutase (SOD), catalase (CAT), and glucose 6 phosphate dehydrogenase (G6PD), whereas the level of glutathione reduced (GSH) was decreased. Some histopathological changes of the kidney tissue including tubular epithelial hypertrophy, vacuolizations, necrotic glomerulus cell, capillaries network shrinking, vascular congestion, interstitial infiltration, loss of apical microvilli, and deteriorated mitochondria were observed in CA group. Concomitant FU administration with CsA enhanced renal function, as indicated by the low level of creatinine. Moreover, FU ameliorated the oxidative status in kidney tissue as well as it provided histological protection against CsA-induced kidney injury. Conclusion: FU can develop a protective mechanism against kidney injury induced by CsA that mediated by OS.

Mangosteen Hinders Gamma Radiation-Mediated Oxidative Stress and Liver Injury by Down-Regulating TNF-α/NF-κB and Pro-Fibrotic Factor TGF-β1 Inducing Inflammatory Signaling

“…Antioxidants could significantly decrease the cellular ROS levels by increasing manganese superoxide dismutase expression that resulted in boosted cell survival. 39 On the other hand, anti-inflammatory drugs have also the capability to renovate cellular organs such as relieving endoplasmic reticulum stress via the inhibition of NF-κB activation and inflammatory response. 40 …”

Analysis of Molecular Interactions between Components in Phospholipid-Immunosuppressant-Antioxidant Mixed Langmuir Films

“…15 The protective role of different antioxidants is also confirmed in CsA-induced hepatotoxicity 16,17 and nephrotoxicity. 18,19 Accordingly, the incorporation of an antioxidant in association with CsA can be an effective way to reduce the undesirable effects of CsA, protect unsaturated PL bonds against oxidation, and consequently reduce the risk of implant rejection. A potential candidate can be one of the derivatives of gallic acid, i.e., lauryl gallate (LG), which in contrast to the former compound is capable of forming the water-insoluble Langmuir monolayers.…”

Experimental study of renal toxicity of cyclosporine and the ameliorative effect of N-acetylecysteine in albino rat

“…From previous studies, antioxidants cause an increase in the antioxidants levels and decrease in the peroxidation and ROS levels which can lead to improvement of the morphological and cytohistological structure of the tissues (Al Khatib et al, 2019).…”