Does silybin protect against toxicity induced by polymyxin E in rat kidney?

Hassan, Sherif S.; Youakim, Magdy; Rizk, A.; Thomann, Charity; Ahmad, Zulfiqar

doi:10.1002/nau.23109

Cited by 12 publications

(17 citation statements)

References 46 publications

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“…BUN and CREA values were elevated in rats treated with OTA. The CURC significantly reduced BUN and CREA values in the serum of rats treated with OTA and this, in accordance with several data in literature, could be due to a reduction in renal damage by the CURC [49][50][51]. The increase in CREA observed in rats treated with OTA is related to the GFR reduction, which is associated with oxygen free radical formation.…”

Section: Discussionsupporting

confidence: 90%

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

et al. 2020

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Ochratoxin A (OTA) is a powerful nephrotoxin and the severity of its damage to kidneys depends on both the dose and duration of exposure. According to the scientific data currently available, the mechanism of action still is not completely clarified, but it is supposed that oxidative stress is responsible for OTA-induced nephrotoxicity. Bioactive compound use has emerged as a potential approach to reduce chronic renal failure. Therefore, curcumin (CURC), due to its therapeutic effects, has been chosen for our study to reduce the toxic renal effects induced by OTA. CURC effects are examined in Sprague Dawley rats treated with CURC (100 mg/kg), alone or in combination with OTA (0.5 mg/kg), by gavage daily for 14 days. The end result of the experiment finds rats treated with OTA show alterations in biochemical and oxidative stress parameters in the kidney, related to a decrease in the Glomerular Filtration Rate (GFR). Conversely, the administration of CURC attenuates oxidative stress and prevents glomerular hyperfiltration versus the OTA group. Furthermore, kidney histological tests show a reduction in glomerular and tubular damage, inflammation and tubulointerstitial fibrosis. This study shows that CURC can mitigate OTA–induced oxidative damage in the kidneys of rats.

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Section: Discussionsupporting

confidence: 90%

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

et al. 2020

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“…The control group (Group I) received no treatment. The vehicle group (Group II) received normal saline (75/25 ratio) with propylene glycol as a vehicle solution (Agri Laboratories Ltd., St. Joseph, MO) intravenously, twice daily for 7 days . The treatment group (Group III) received polymyxin E, which was prepared from colistin sulfate (Zhejiang Shenghua Biology Co., Ltd., Zhejiang, China) according to Li et al A collective dose of 36.5 mg/kg polymyxin E was given intravenously twice daily, 8 h apart from each other, for 7 days .…”

Section: Methodsmentioning

confidence: 99%

“…This dose is equivalent to the dose producing nephrotoxicity in humans . The protection group (Group IV) received polymyxin E in the same dose that was used in Group III, but it was also given 50 mg/kg of silybin in the form of silymarin (Sigma‐Aldrich Chemical Co., Ltd., Cairo, Egypt) intravenously, for 7 days. The silybin was given twice daily, preceding the two doses of polymyxin E by 2 h .…”

Section: Methodsmentioning

confidence: 99%

“…Specifically, the aim of the present study was to assess whether silybin could decrease elevated urine and serum kidney functions induced by polymyxin E in rat kidney. We used biochemical analysis of urine and serum to verify a previous study by Hassan et al that suggested silybin could restore structural damage induced by polymyxin E in rat kidney.…”

Section: Introductionmentioning

confidence: 95%

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Possible protective role of silybin against polymyxin E‐induced toxic effect in rat kidneys: A biochemical approach

Hassan¹,

Thomann

Ettarh³

et al. 2017

Neurourology and Urodynamics

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Group III results suggested an affection of the renal glomeruli and tubules, and Group IV results suggested a possible protective effect of silybin against polymyxin E-induced nephrotoxicity. Additional studies are recommended that use different doses of silybin for Groups III and IV to test for statistical differences for kidney functions and that test the protective effect of silybin against nephrotoxicity induced by polymyxin E in humans.

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“…Throughout the world, there seems a steady increase and interest in the use of natural products as antimicrobial agents individually or in combination with other such molecules [12, 24–29]. Numerous phytochemicals have been shown to have dietary benefits and are potential antitumor or antimicrobial agents [30–33]. …”

Section: Introductionmentioning

confidence: 99%

Safranal and its analogs inhibit Escherichia coli ATP synthase and cell growth

Liu

Amini

Ahmad

2017

International Journal of Biological Macromolecules

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Safranal, a dominant component of saffron, is known to have antitumor, cytotoxic, and antibacterial properties. In this study, we examined safranal and its structural analogs— thymol, carvacrol, damascenone, cuminol, 2,6,6-Trimethyl-2-cyclohexene-1,4-dione (TMCHD), 4-Isopropylbenzyl bromide (IPBB), and 4-tert-Butylphenol (TBP) induced inhibition of Escherichia coli membrane bound F1Fo ATP synthase. Safranal and its analogs inhibited wild-type enzyme to variable degrees. While safranal caused 100% inhibition of wild-type F1Fo ATP synthase only, about 50% inhibition occurred for αR283D mutant ATP synthase. Moreover, safranal, thymol, carvacrol, damascenone, cuminol, TMCHD, IPBB, and TBP all fully abrogated the growth of wild-type E. coli cells and had partial or no effect on the growth of null and mutant E. coli strains. Therefore, the antimicrobial properties of safranal, thymol, carvacrol, damascenone, cuminol, TMCHD, IPBB, and TBP can be linked to their binding and inhibition of ATP synthase. Total loss of growth in wild-type and partial or no growth loss in null or mutant E. coli strains demonstrates that ATP synthase is a molecular target for safranal and its structural analogs. Partial inhibition of the αArg-283 mutant enzyme establishes that αArg-283 residue is required in the polyphenol binding pocket of ATP synthase for the binding of safranal. Furthermore, partial growth loss for the null and mutant strains in the presence of inhibitors also suggests the role of other targets and residues in the process of inhibition.

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Does silybin protect against toxicity induced by polymyxin E in rat kidney?

Cited by 12 publications

References 46 publications

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

Possible protective role of silybin against polymyxin E‐induced toxic effect in rat kidneys: A biochemical approach

Safranal and its analogs inhibit Escherichia coli ATP synthase and cell growth

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