Nephroprotective efficacy of ceftriaxone against cisplatin-induced subchronic renal fibrosis in rats

Abdel‐Daim, Mohamed M.; El‐Sayed, Yasser S.; Eldaim, Mabrouk Attia Abd; Ibrahim, Abdelazim

doi:10.1007/s00210-016-1332-5

Cited by 27 publications

(11 citation statements)

References 51 publications

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“…Therefore, rutin can protect the kidney from CP-induced injury via improvement in oxidant status. A similar study found that rutin pre-treatment attenuates renal inflammation and apoptosis induced by cisplatin through reducing TNF-α, NF k B and caspase-3 levels [18, 25]. …”

Section: Discussionmentioning

confidence: 99%

“…Cisplatin damages the DNA resulting in apoptosis induction [18]. In response to cisplatin, several signaling pathways, which can be activated by lipid peroxidation and oxidative stress, modulate the cell survival or apoptosis [18, 19].…”

Section: Introductionmentioning

confidence: 99%

“…In response to cisplatin, several signaling pathways, which can be activated by lipid peroxidation and oxidative stress, modulate the cell survival or apoptosis [18, 19]. The mitogen-activated protein kinase ( MAPK ) pathways regulate differentiation, proliferation, apoptosis and are activated by chemical and physical stresses [20].…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of rutin supplementation against cisplatin-induced Nephrotoxicity in rats

et al. 2017

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BackgroundCisplatin (CP) is commonly used in the treatment of different types of cancer but nephrotoxicity has been a major limiting factor. Therefore, the present study aimed to study the possible protective effect of rutin against nephrotoxicity induced by cisplatin in rats.MethodsForty male Wistar albino rats were randomly divided into 4 groups. Rats of group 1 control group intraperitoneal (i.p.) received 2.5 ml/kg, group 2 CP group received single dose 5 mg/kg cisplatin i.p. group 3 rutin group orally received 30 mg/kg rutin group 4 (CP plus rutin) received CP and rutin as in group 2 and 3. Kidneys were harvested for histopathology and for the study the gene expression of c-Jun N-terminal kinases (JNK), Mitogen-activated protein kinase 4 (MKK4), MKK7, P38 mitogen-activated protein kinases (P38), tumor necrosis factors alpha (TNF-α), TNF Receptor-Associated Factor 2 (TRAF2), and interleukin-1 alpha (IL-1-α).ResultsThe cisplatin single dose administration to rats induced nephrotoxicity associated with a significant increase in blood urea nitrogen (BUN) and serum creatinine and significantly increase Malondialdehyde (MDA) in kidney tissues by 230 ± 5.5 nmol/g compared to control group. The animal treated with cisplatin showed a significant increase in the expression levels of the IL-1α (260%), TRFA2 (491%), P38 (410%), MKK4 (263%), MKK7 (412%), JNK (680%) and TNF-α (300%) genes compared to control group. Additionally, histopathological examination showed that cisplatin-induced interstitial congestion, focal mononuclear cell inflammatory, cell infiltrate, acute tubular injury with reactive atypia and apoptotic cells. Rutin administration attenuated cisplatin-induced alteration in gene expression and structural and functional changes in the kidney. Additionally, histopathological examination of kidney tissues confirmed gene expression data.ConclusionThe present study suggested that the anti-oxidant and anti-inflammatory effect of rutin may prevent CP-induced nephrotoxicity via decreasing the oxidative stress, inhibiting the interconnected ROS/JNK/TNF/P38 MAPK signaling pathways, and repairing the histopathological changes against cisplatin administration.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protective effect of rutin supplementation against cisplatin-induced Nephrotoxicity in rats

et al. 2017

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“…Therefore, the appropriate regulation of fibrotic changes by cancer-related factors and anti-cancer therapies is important for the maintenance of homeostasis and to improve the prognosis in patients with cancer. Indeed, many investigators have specifically investigated the molecular mechanisms and preventive strategies of fibrosis in various organs [ 77 , 78 ].…”

Section: Activity Of Royal Jelly Against Cancer Therapy-induced Tomentioning

confidence: 99%

Anti-Cancer and Protective Effects of Royal Jelly for Therapy-Induced Toxicities in Malignancies

Miyata

Sakai

2018

IJMS

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Royal jelly (RJ) is a glandular secretion produced by worker honeybees and is a special food for the queen honeybee. It results in a significant prolongation of the lifespan of the queen honeybee compared with the worker honeybees through anti-inflammatory, anti-oxidant and anti-microbial activities. Consequently, RJ is used as cosmetic and dietary supplement throughout the world. In addition, in vitro studies and animal experiments have demonstrated that RJ inhibits cell proliferation and stimulates apoptosis in various types of malignant cells and affects the production of various chemokines, anti-oxidants and growth factors and the expression of cancer-related molecules in patients with malignancies, especially in patients treated with anti-cancer agents. Therefore, RJ is thought to exert anti-cancer effects on tumor growth and exhibit protective functions against drug-induced toxicities. RJ has also been demonstrated to be useful for suppression of adverse events, the maintenance of the quality of life during treatment and the improvement of prognosis in animal models and patients with malignancies. To understand the mechanisms of the beneficial effects of RJ, knowledge of the changes induced at the molecular level by RJ with respect to cell survival, inflammation, oxidative stress and other cancer-related factors is essential. In addition, the effects of combination therapies of RJ and other anti-cancer agents or natural compounds are important to determine the future direction of RJ-based treatment strategies. Therefore, in this review, we have covered the following five issues: (1) the anti-cancer effects of RJ and its main component, 10-hydroxy-2-decenoic acid; (2) the protective effects of RJ against anti-cancer agent-induced toxicities; (3) the molecular mechanisms of such beneficial effects of RJ; (4) the safety and toxicity of RJ; and (5) the future directions of RJ-based treatment strategies, with a discussion on the limitations of the study of the biological activities of RJ.

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“…Parsley oil, with its antioxidant activity, used in the treatment of cisplatin-induced hepatic and cardiac injuries [ 29 ]. Other study found that ceftriaxone displayed protective efficacy against cisplatin-induced renal tubule-interstitial fibrosis, possibly via anti-fibrotic potential [ 30 ]. Other natural product such as honey bee and royal jelly could be used as dietary preventive natural products against subchronic cisplatin-induced renal injury [ 31 ].…”

Section: Introductionmentioning

confidence: 99%

Neuro-protective effect of rutin against Cisplatin-induced neurotoxic rat model

Almutairi

Alanazi

Alshammari

et al. 2017

BMC Complement Altern Med

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BackgroundCisplatin is widely used chemotherapeutic agent for cancer treatment with limited uses due to its neurotoxic side effect. The aim of this study was to determine the potential preventive effects of rutin on the brain of cisplatin- neurotoxic rat model.MethodsForty rats were divided into four groups. Group-1 (control group) was intra-peritoneal (IP) injected with 2.5 ml/kg saline. Group-2 (rutin group) was orally administrated 30 mg/kg rutin dissolved in water for 14 days. Group-3 (cisplatin group) was IP received 5 mg/kg cisplatin single dose. Group-4 (rutin and cisplatin group) was orally administrated 30 mg/kg rutin dissolved in water for 14 days with a single dose of 5 mg/kg cisplatin IP on day ten. Brain tissues from frontal cortex was used to extract RNA, the gene expression levels of paraoxonase-1 (PON-1), PON-2, PON-3, peroxisome proliferator-activated receptor delta (PPAR-δ), and glutathione peroxidase (GPx) was investigated by Real-time PCR.ResultsCisplatin significantly decreased the expression levels of PON-1, PON-3, PPAR-δ and GPX whereas significantly increased PON-2 expression levels. Co-administration of Rutin prevented the cisplatin-induced toxicity by restoring the alteration in the studied genes to normal values as in the control group.ConclusionThis study showed that Rutin has neuroprotective effect and reduces cisplatin- neurotoxicity with possible mechanism via the antioxidant pathway.

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Nephroprotective efficacy of ceftriaxone against cisplatin-induced subchronic renal fibrosis in rats

Cited by 27 publications

References 51 publications

Protective effect of rutin supplementation against cisplatin-induced Nephrotoxicity in rats

Protective effect of rutin supplementation against cisplatin-induced Nephrotoxicity in rats

Anti-Cancer and Protective Effects of Royal Jelly for Therapy-Induced Toxicities in Malignancies

Neuro-protective effect of rutin against Cisplatin-induced neurotoxic rat model

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