Protective Effect of Docosahexaenoic Acid Against Cyclosporine A-Induced Nephrotoxicity in Rats: A Possible Mechanism of Action

Mariee, Amr D.; Abd-Ellah, Mohamed F.

doi:10.3109/0886022x.2010.541584

Cited by 14 publications

(11 citation statements)

References 51 publications

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“…Similarly, many studies [28][29][30] have clearly shown that FO has radicalscavenging and anti-oxidant properties, and that it could be used against oxidative effects of many toxic agents, such as CP. A study 30 about FO use against CP toxicity demonstrated that FO treatment ameliorated specific CP-induced histological alterations and oxidative damage in rat kidney tissue.…”

Section: Oxidative and Histological Changesmentioning

confidence: 97%

Fish oil protects the peripheral and central nervous systems against cisplatin-induced neurotoxicity

Kamışlı

Çiftçi

Çetin

et al. 2013

Nutritional Neuroscience

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Section: Oxidative and Histological Changesmentioning

confidence: 97%

Fish oil protects the peripheral and central nervous systems against cisplatin-induced neurotoxicity

Kamışlı

Çiftçi

Çetin

et al. 2013

Nutritional Neuroscience

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“…In addition, CsA also blocks the formation of nitric oxide, thereby increasing the damage caused by oxidative stress. Blocking the expression of nuclear factor-κB (NF-κB) reduces the production of reactive oxidative metabolites and improves kidney antioxidant capacity (5,6). Curcumin (Cur) has been reported to increase the proliferation, reduce the rate of apoptosis and reduce the Bcl-2-associated X (Bax)/Bcl-2 ratio in human umbilical vein endothelial cells (7).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of curcumin against cyclosporine A‑induced rat nephrotoxicity

et al. 2018

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This study explored the potential value of curcumin, a natural product, in the protection of CsA‑induced nephrotoxicity. The aim of the present study was to investigate the effects of curcumin on Cyclosporine A (CsA)‑induced renal oxidative stress and determine the potential underlying molecular mechanisms of the renal protective effects of Cur. HK‑2 human renal cells were co‑treated with CsA and various doses of Cur. Cell survival rate was determined by an MTT assay, total cellular protein was collected and oxidative stress in cell homogenates was evaluated by determining the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH‑Px) and catalase (CAT), the levels of malondialdehyde (MDA) and reactive oxygen species (ROS), and total antioxidant capacity. Furthermore, Bcl‑2 and Bcl‑2‑associated X (Bax) protein expression was measured by western blot analysis. In addition, a CsA‑induced nephrotoxicity (CAN) rat model was also established. Renal function was analyzed by measuring creatinine (Crea) and blood urea nitrogen (BUN) in the serum of rats, and histopathological examination was performed on renal tissues using hematoxylin and eosin staining, periodic acid‑Schiff staining and nuclear factor‑κB (NF‑κB) immunostaining. The results demonstrated that treatment of HK‑2 cells with CsA significantly increased ROS and MDA levels, and decreased the activities of SOD, GSH‑Px and CAT, compared with the control group. However, these effects of CsA were dose‑dependently improved by treatment with Cur. In addition, Cur treatment increased Bcl‑2 and decreased Bax protein in HK‑2 cells, compared with cells treated with CsA alone. In the CAN rat model CsA (30 mg/kg) treatment significantly elevated serum Crea levels and BUN, but lowered endogenous Crea clearance rate, compared with the control group. Co‑administration of Cur with CsA significantly reversed the effects of CsA on serum Crea levels, BUN and Crea clearance rate (Ccr). Additionally, Cur alleviated CsA‑induced renal cell injury, as less vacuolar degeneration of glomerular cells was observed compared with the CsA alone group. In conclusion, Cur may increase renal antioxidant capacity and reduce the Bax/Bcl‑2 ratio, subsequently improving CsA‑induced renal failure and renal tubular deformation and cell vacuolization.

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“…Our results suggested that NO prevented renal cells from CsA-induced apoptosis in vivo. Other data suggested that docosahexaenoic acid had a protective effect on CsA nephrotoxicity through increasing total NO bioavailability in rat renal tissues [72]. NO could modulate vascular endothelial growth factor and its receptors.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Cyclosporine-Induced Renal Cell Apoptosis: A Systematic Review

Xiao

Shan

et al. 2012

Am J Nephrol

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Background/Aims: Chronic cyclosporine A (CsA) nephrotoxicity (CCN) is an important cause of chronic renal dysfunction with no effective clinical intervention. To further elucidate the mechanisms of renal cell apoptosis in CCN, all relevant in vivo studies on this subject were analyzed. Methods: We searched for in vivo studies on the mechanisms of CsA-induced renal cell apoptosis in Medline (1966–July 2010), Embase (1980–July 2010) and ISI (1986–July 2010). The studies were evaluated for their quality according to a set of in vivo standards, data extracted according to PICOS, and then synthesized. Results: Renal cell apoptosis was an important feature of CCN and an important factor of renal dysfunction. First, CsA could upregulate Fas/Fas ligand, downregulate Bcl-2/Bcl-XL, and increase caspase-1 and caspase-3. Second, it could induce oxidative stress and damage the antioxidant defense system. Third, it could increase endoplasmic reticulum stress protein in a dose- and time-dependent manner. Fourth, CsA could impair the urine concentration and decrease the expression of hypertonicity-induced genes. Fifth, CsA-induced renal cell apoptosis was significantly decreased by blocking the angiotensin II type 1 receptor using losartan. Conclusions: The in vivo mechanisms for CCN are more complex than those found in vitro. CsA can induce renal cell apoptosis using five pathways in vivo and activated caspases might be the ultimate intersection of these pathways and the common intracellular pathway mediating apoptosis. These data provide new potential points for intervention and need to be confirmed by further studies.

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Protective Effect of Docosahexaenoic Acid Against Cyclosporine A-Induced Nephrotoxicity in Rats: A Possible Mechanism of Action

Cited by 14 publications

References 51 publications

Fish oil protects the peripheral and central nervous systems against cisplatin-induced neurotoxicity

Fish oil protects the peripheral and central nervous systems against cisplatin-induced neurotoxicity

Protective effect of curcumin against cyclosporine A‑induced rat nephrotoxicity

Mechanisms of Cyclosporine-Induced Renal Cell Apoptosis: A Systematic Review

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