Renal protective effects of arjunolic acid in a cisplatin-induced nephrotoxicity model

Elsherbiny, Nehal M.; Eladl, Mohamed Ahmed; Al‐Gayyar, Mohammed M.H.

doi:10.1016/j.cyto.2015.10.010

Cited by 43 publications

(27 citation statements)

References 48 publications

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“…The results of the present study revealed that caspase-9 level was induced in cis-treated mice. These results are in agreement with other studies 67,68 . A previous study reported that apoptotic cell death in renal tubule cell was caused by cis through the generation of reactive oxygen species, which activate the pro-apoptotic Bcl-2 family member Bax, which as a consequence induces mitochondrial permeability transition, causing the release of cytochrome c, caspase-9 activation, and entry into the apoptosis execution phase 69 .…”

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confidence: 94%

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2018

IJPSR

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The present study aimed to investigate the anticancer effect of rosmarinic acid (RA), both alone and in combination with cisplatin (cis). Also, the potential nephroprotective effects of RA against cis-induced nephrotoxicity in mice and the possible mechanisms underlying this protection were explored. Treatment of HepG2 cells with RA produced a significant decline in cellular proliferation. RA induced cell cycle arrest at G 0 / G 1 phase and S phase, significantly inhibited vascular endothelial growth factor (VEGF) concentration and induced caspase-3 level in cell lysate. While pre-treatment with IC 50 RA before cis addition significantly enhanced cis cytotoxic activity in HepG2 cells. Moreover, Pre-treatment with RA significantly mitigated cis-induced elevation of blood urea nitrogen (BUN) and serum creatinine levels. The elevated levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), Bax and caspase-9 in kidney tissues were significantly reversed. Additionally, RA significantly abrogated cis-induced reduction in reduced glutathione level (GSH). The histopathological examination emphasized the obtained results. Conclusion: RA possesses cytotoxic activity against HepG2 cell line through cell cycle arrest, induction of caspase-3 and inhibition of VEGF. In addition, RA enhances cis-induced cytotoxicity in HepG2 cells. Also, it ameliorates cis-induced nephrotoxicity in mice; an effect which could be attributed to inhibition of oxidative stress, inflammation and apoptosis.

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confidence: 94%

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2018

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“…Relationships among renal morphology, the serum levels of inflammatory mediators, and the state of cell apoptosis were found. The pathogenesis and progression of I/R injury are influenced by the proinflammatory cytokines, including IL-1β, IL-6, MCP-1, and TNF-α [23,24]. DEX not only acts locally on the kidney's α 2 -adrenoceptors but also influences the anti-inflammatory reactions, thereby mitigating the damaging effects of I/R on the kidney.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine Protects against Ischemia and Reperfusion-Induced Kidney Injury in Rats

Bao

Dai

2020

Mediators of Inflammation

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Acute kidney injury (AKI), a clinical syndrome, is a sudden onset of kidney failure that severely affects the kidney tubules. One potential treatment is dexmedetomidine (DEX), a highly selective α2-adrenoreceptor agonist that is used as an anesthetic adjuvant. It also has anti-inflammatory, neuroprotective, and sympatholytic qualities. The aim of this study was to establish whether DEX also offers protection against ischemia and reperfusion- (I/R-) induced AKI in rats. An intraperitoneal injection of DEX (25 μg/kg) was administered 30 min prior to the induction of I/R. The results indicate that in the I/R rats, DEX played a protective role by reducing the damage to the tubules and maintaining renal function. Furthermore, in response to I/R, the DEX treatment reduced the mRNA expression of TNF-α, IL-1β, IL-6, and MCP-1 in the kidney tissues and the serum levels of TNF-α, IL-1β, IL-6, and MCP-1. DEX also reduced the levels of oxidative stress and apoptosis in the tubular cells. These results indicate that in response to I/R kidney injury, DEX plays a protective role by inhibiting inflammation and tubular cell apoptosis, reducing the production of reactive oxygen species, and promoting renal function.

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“…8 Nephrotoxicity occurs by renal toxic effects of cisplatin, but the underlying mechanism is not fully understood. 6 It is proposed that renal cell injury is related to the drug accumulated in kidneys (renal tubular cells), causing direct inflammation, generation of reactive oxygen species (ROS), DNA damage, mitochondrial dysfunction, and apoptosis. 5,6,9,10 Despite large number of studies about this topic, none of them is proved to be completely effective.…”

Section: Introductionmentioning

confidence: 99%

“…6 It is proposed that renal cell injury is related to the drug accumulated in kidneys (renal tubular cells), causing direct inflammation, generation of reactive oxygen species (ROS), DNA damage, mitochondrial dysfunction, and apoptosis. 5,6,9,10 Despite large number of studies about this topic, none of them is proved to be completely effective. For example, selenium, melatonin, vitamins C and E, mannitol, and arjunolic acid may be used to prevent or attenuate cisplatin-induced nephrotoxicity.…”

Section: Introductionmentioning

confidence: 99%

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Potential of morin and hesperidin in the prevention of cisplatin-induced nephrotoxicity

Kaltalıoğlu

Cevher

2016

Renal Failure

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Oxidative stress is one of the important mechanisms of cisplatin-induced nephrotoxicity. Therefore, this study was designed to explore the potential protective effects of morin and/or hesperidin on oxidative stress in cisplatin-induced nephrotoxicity. This study was performed on 42 Wistar rats. Rats were divided into seven groups: control, morin, hesperidin, cisplatin, cisplatin þ morin, cisplatin þ hesperidin, and cisplatin þ morin þ hesperidin. Morin and/or hesperidin were given for 10 consecutive days by oral gavage and on the 4th day a single dose of cisplatin (7 mg/kg) was injected intraperitoneally. After administrations, on the 11th day of the experiment the animals were killed, and malondialdehyde (MDA), nitric oxide (NOx), glutathione (GSH) levels and myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD) activity were measured. Cisplatin-treated rats showed increased levels of MDA, and decreased levels of NOx also activity of CAT. Morin and/or hesperidin pretreatment prevent oxidative stress in kidney tissue, while they increase the NOx level, CAT activity, and decrease MPO activity. In conclusion, morin þ hesperidin pretreatment may have a significant potential for protection of cisplatin-induced nephrotoxicity.ARTICLE HISTORY

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Renal protective effects of arjunolic acid in a cisplatin-induced nephrotoxicity model

Cited by 43 publications

References 48 publications

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Dexmedetomidine Protects against Ischemia and Reperfusion-Induced Kidney Injury in Rats

Potential of morin and hesperidin in the prevention of cisplatin-induced nephrotoxicity

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