The protective effect of pomegranate extract against cisplatin toxicity in rat liver and kidney tissue

Bakır, Salih; Yazgan, Ümit Can; İbiloğlu, İbrahim; Elbey, Bilal; Kızıl, Murat; Kelle, Mustafa

doi:10.3109/13813455.2015.1068336

Cited by 24 publications

(16 citation statements)

References 30 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increasing the concentration of cisplatin is the most common strategy to offset cisplatin resistance. However, high-dose cisplatin may cause severe liver toxicity, which is the main side-effect of cisplatin therapy (36,37). In the present study we demonstrated that vandetanib was as effective as high-dose cisplatin in impairing cisplatin-resistant NB subcutaneous tumor growth in vivo.…”

Section: Discussionsupporting

confidence: 53%

Vandetanib inhibits cisplatin‑resistant neuroblastoma tumor growth and invasion

Yang

Wei

2018

Oncol Rep

View full text Add to dashboard Cite

Resistance is the major cause of cisplatin treatment failure in neuroblastoma (NB). Vandetanib is widely used in the treatment of several cancers. In the present study, we aimed to determine the potential of vandetanib in cisplatin‑resistant NB therapy. Immunohistochemistry (IHC) staining was employed to detect p‑RET and CXCR4 expression in cisplatin‑resistant or ‑sensitive NB tissues from patients. Vandetanib was added to treat selected cisplatin‑resistant SH‑SY5Y cells (SH‑SY5Y‑R); this was followed by CCK8 assay, colony formation assay, and invasion assay. Furthermore, the effect of vandetanib on subcutaneous tumor growth was investigated in mice. Our results demonstrated greater expression of p‑RET and CXCR4 in cisplatin‑resistant neuroblastomas (NBs). Vandetanib significantly inhibited SH‑SY5Y‑R cell proliferation, colony formation, and invasion, while downregulating p‑RET and CXCR4 expression. Furthermore, vandetanib was as effective as high‑dose cisplatin in impairing cisplatin‑resistant NB subcutaneous tumor growth. Notably, vandetanib caused less severe liver toxicity in mice compared with high‑dose cisplatin. In summary, this study identified Vandetanib as a potential drug for cisplatin‑resistant NB treatment.

show abstract

Section: Discussionsupporting

confidence: 53%

Vandetanib inhibits cisplatin‑resistant neuroblastoma tumor growth and invasion

Yang

Wei

2018

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…Harm to liver cells can cause escape into the serum owing to autolytic breakdown or cellular necrosis [ 52 ]. There are also some earlier studies suggesting escalated serum ALT and AST levels related to increased ROS [ 53 , 54 ]. Enhanced levels of CRE and BUN can be attributed to retention of Cis in terminal collecting duct, the distal nephron of kidneys.…”

Section: Discussionmentioning

confidence: 93%

“…There are many studies indicating the relation between oxidative stress, MDA, and Cis-induced liver and kidney toxicity [ 49 , 50 , 53 ]. MDA is one of the basic indicators of oxidative harm and has been considered to take a significant part in the toxicity of several xenobiotics.…”

Section: Discussionmentioning

confidence: 99%

“…MDA is one of the basic indicators of oxidative harm and has been considered to take a significant part in the toxicity of several xenobiotics. Many pathophysiological systems have been put forward to clarify the enhanced MDA and reduced antioxidant levels in Cis toxicity [ 19 , 40 , 50 , 53 ]. The data obtained from present study affirm that acute intoxication with Cis leads to an important elevation of MDA concentration in the liver.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Protective Effect of Naringenin-Oxime on Cisplatin-Induced Toxicity in Rats

Koyuncu

Koçyiğit

Gönel

et al. 2017

Biochemistry Research International

View full text Add to dashboard Cite

The aim of this study is to examine the protective effect of naringenin-oxime (NOX) on cisplatin-induced major organ toxicity and DNA damage in rats. Thirty-five male Wistar albino rats were equally split into five groups as follows: control (i.p., 0.1 ml of saline), Cis administration (i.p., 7 mg/kg b.w.), NOX treatment (i.p., 20 mg/kg b.w., daily for ten days), Cis + NOX20, and Cis + NOX40 combination (i.p., 20 and 40 mg/kg b.w., daily for ten days). Serum and peripheral blood mononuclear leukocytes (PBMC) were obtained from blood. Malondialdehyde, glutathione, total antioxidant and oxidant status, and catalase were measured in serum, liver, and kidney, and oxidative stress index was calculated. In parallel, paraoxonase and arylesterase activities were tested in liver and serum. We used 8-OHdOG as a marker for DNA damage in serum via ELISA and in PMBC via comet assay. Treatment with Cis elevated the levels of serum biochemical parameters, oxidative stress, and DNA damage. Pretreatments of NOX restored biochemical and oxidative stress parameters in serum, renal, and liver tissues (p < 0.01) and reduced 8-OHdG level, a finding further supported by comet assay in PBMC. Observations of the present study support the fact that treatment with NOX prevents Cis-induced hepatotoxicity, nephrotoxicity, and genotoxicity by restoring antioxidant system.

show abstract

“…In addition, dysregulation of MAPK signaling pathways has been demonstrated in acute and chronic kidney disease induced by cisplatin [7]. Compounds isolated from natural sources, such as Artemisia asiatica , pomegranate, and Chrysanthemum indicum , have been shown to reduce the nephrotoxicity due to cisplatin [8], [9], [10], [11], [12].…”

Section: Introductionmentioning

confidence: 99%

Protective effect of ginsenoside Rh3 against anticancer drug-induced apoptosis in LLC-PK1 kidney cells

Lee

Kang

2017

Journal of Ginseng Research

View full text Add to dashboard Cite

BackgroundGinsenosides are active components of Panax ginseng that exert various health benefits including kidney protection effect. The medicinal activity of ginsenosides can be enhanced by modulating their stereospecificity by heat processing. Ginsenosides Rk2 and Rh3 represent positional isomers of the double bond at C-20(21) or C-20(22).MethodsThe present study investigated the kidney-protective effects of ginsenosides Rk2 and Rh3 against cisplatin, a platinum based anticancer drug, induced apoptotic damage in renal proximal LLC-PK1 cells.ResultsAs a result, ginsenoside Rh3 shows a stronger protective effect than that shown by Rk2. Cisplatin-induced elevated protein levels of phosphorylated c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), p38, and cleaved caspase-3 decreased after cotreatment with ginsenoside Rh3. The increase in the percentage of apoptotic LLC-PK1 cells induced by cisplatin treatment also significantly reduced after cotreatment with ginsenoside Rh3.ConclusionThese results demonstrate that inhibition of the JNK and ERK mitogen-activated protein kinase signaling cascade plays a critical role in mediating the renoprotective effect of ginsenoside Rh3.

show abstract

The protective effect of pomegranate extract against cisplatin toxicity in rat liver and kidney tissue

Abstract: In conclusion, these results demonstrate that the anti-oxidant pomegranate juice might have a protective effect against cisplatin-induced toxicity in rat kidney, but not in liver. Pomegranate juice could be beneficial as a dietary supplement in patients receiving chemotherapy medications.

Cited by 24 publications

References 30 publications

Vandetanib inhibits cisplatin‑resistant neuroblastoma tumor growth and invasion

Vandetanib inhibits cisplatin‑resistant neuroblastoma tumor growth and invasion

The Protective Effect of Naringenin-Oxime on Cisplatin-Induced Toxicity in Rats

Protective effect of ginsenoside Rh3 against anticancer drug-induced apoptosis in LLC-PK1 kidney cells

Contact Info

Product

Resources

About