scholarly journals Effect of oleuropein against chemotherapy drug-induced histological changes, oxidative stress, and DNA damages in rat kidney injury

2017 ◽  
Vol 25 (2) ◽  
pp. 447-459 ◽  
Author(s):  
Fatime Geyikoglu ◽  
Murat Emir ◽  
Suat Colak ◽  
Kubra Koc ◽  
Hasan Turkez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Kidney ◽  
Kidney Injury ◽  
Drug Induced ◽  
Histological Changes ◽  
Dna Damages ◽  
Chemotherapy Drug

scholarly journals In Vivo Antioxidant And Kidney Protective Potential Of Atorvastatin In Rat Cadmium-Induced Toxicity

2021 ◽  
Author(s):  
Esmaeil Karami ◽  
Zahra Goodarzi ◽  
Ali Ghanbari ◽  
Ahmad Reza Bandegi ◽  
Sedighe Yosefi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Biochemical Parameters ◽  
Cadmium Chloride ◽  
Rat Kidney ◽  
Intraperitoneal Administration ◽  
Kidney Injury ◽  
Protective Role ◽  
Histological Changes ◽  
Male Wistar Rats

Abstract Purpose: Environmental and occupational exposure to cadmium chloride is known to cause nephrotoxicity linked with oxidative stress in humans and animals. This study used Atorvastatin to examine its effect on cadmium chloride-induced nephrotoxicity in rat model using biochemical and histological methodologies.Methods: Experiments were performed on 56 adult male Wistar rats (200 ±20 g), randomly assigned to eight groups. Atorvastatin was administered by oral for 15 days at 20 mg/kg/day, started 7 days before cadmium chloride intraperitoneal administration (1, 2, and 3 mg/kg) for eight days. On day 16, blood samples were collected, and kidneys were excised to evaluate the biochemical and histopathological changes.Cadmium chloride significantly increased malondialdehyde (MDA), serum creatinine (Cr), blood urea nitrogen (BUN), and decreased superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GPx) levels. Results: Administration of Atorvastatin (20 mg/kg) significantly improved lipid peroxidation, glutathione and activities of antioxidant enzymes and significantly decreased BUN and Creatinine. Atorvastatin clearly improved the histological changes, demonstrating its protective role against Cadmium chloride-induced kidney injury.Conclusion: Treatment with Atorvastatin significantly improves all biochemical parameters and suggests a protecting role against cadmium chloride-induced oxidative stress and histological changes in rat kidney.

scholarly journals Antioxidant Activity, Phenolic Profile, and Nephroprotective Potential of Anastatica hierochuntica Ethanolic and Aqueous Extracts against CCl4-Induced Nephrotoxicity in Rats

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2973
Author(s):  
Tariq I. Almundarij ◽  
Yousef M. Alharbi ◽  
Hassan A. Abdel-Rahman ◽  
Hassan Barakat
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Therapeutic Agent ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Total Phenolic ◽  
Drug Induced ◽  
Total Carotenoids ◽  
Phenolic Profile ◽  
Better Than

Kaff-e-Maryam (Anastatica hierochuntica L.) is extensively used to treat a range of health problems, most notably to ease childbirth and alleviate reproductive system-related disorders. This study aimed to evaluate the effect of A. hierochuntica ethanolic (KEE), and aqueous (KAE) extracts on CCl4-induced oxidative stress and nephrotoxicity in rats using the biochemical markers for renal functions and antioxidant status as well as histopathological examinations of kidney tissue. A. hierochuntica contained 67.49 mg GAE g−1 of total phenolic compounds (TPC), 3.51 µg g−1 of total carotenoids (TC), and 49.78 and 17.45 mg QE g−1 of total flavonoids (TF) and total flavonols (TFL), respectively. It resulted in 128.71 µmol of TE g−1 of DPPH-RSA and 141.92 µmol of TE g−1 of ABTS-RSA. A. hierochuntica presented superior antioxidant activity by inhibiting linoleic acid radicals and chelating oxidation metals. The HPLC analysis resulted in 9 and 21 phenolic acids and 6 and 2 flavonoids in KEE and KAE with a predominance of sinapic and syringic acids, respectively. Intramuscular injection of vit. E + Se and oral administration of KEE, KAE, and KEE + KAE at 250 mg kg−1 body weight significantly restored serum creatinine, urea, K, total protein, and albumin levels. Additionally, they reduced malondialdehyde (MOD), restored reduced-glutathione (GSH), and enhanced superoxide dismutase (SOD) levels. KEE, KAE, and KEE + KAE protected the kidneys from CCl4-nephrotoxicity as they mainly attenuated induced oxidative stress. Total nephroprotection was about 83.27%, 97.62%, and 78.85% for KEE, KAE, and KEE + KAE, respectively. Both vit. E + Se and A. hierochuntica extracts attenuated the histopathological alteration in CCl4-treated rats. In conclusion, A. hierochuntica, especially KAE, has the potential capability to restore oxidative stability and improve kidney function after CCl4 acute kidney injury better than KEE. Therefore, A. hierochuntica has the potential to be a useful therapeutic agent in the treatment of drug-induced nephrotoxicity.

scholarly journals Purified Sika deer antler protein attenuates GM-induced nephrotoxicity by activating Nrf2 pathway and inhibiting NF-κB pathway

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhenyi Wang ◽  
Lulu Wang ◽  
Jing Wang ◽  
Jiacheng Luo ◽  
Haonan Ruan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Sika Deer ◽  
Kidney Injury ◽  
Annexin V ◽  
Expression Level ◽  
Hek293 Cells ◽  
Protective Effects ◽  
Deer Antler ◽  
Drug Induced

Abstract Although gentamicin is widely used as an antibiotic in clinical practice, it also has some side-effects, such as acute kidney injury, which is a common condition caused by the abuse of gentamicin. Sika deer antler protein (SDAPR) can antagonize drug-induced AKI. Since SDAPR is recognized as an effective part of velvet antler, its components were further separated. Two components named SDAP1 and SDAP2 were obtained. The protective effects of SDAPR, SDAP1 and SDAP2 on GM-induced cytotoxicity to HEK293 and its potential mechanisms were studied. MTT and xCELLigence Real-Time cell analysis showed that SDAPR, SDAP1 and SDAP2 could protect HEK293 cells from GM toxicity. Similarly, SDAPR, SDAP1 and SDAP2 can reduce ROS level, reduce oxidative stress and improve inflammation Further studies have shown that SDAPR, SDAP1 and SDAP2 upregulate the Nrf2/HO-1 pathway by increasing the expression of Nrf2 and HO-1, and down-regulate the NF-κB pathway by reducing the protein expression of NF-κB. Annexin V/PI flow cytometry and Hoechst 33258 staining showed that SDAPR, SDAP1 and SDAP2 inhibited GM-induced apoptosis in HEK293 cells. Western blot analysis showed SDAPR, SDAP1 and SDAP2 decreased expression level of Bax and Cleaved-caspase-3, and increased the expression level of Bcl-2. In addition, we examined the feasibility of SDAP1 and SDAP1 to avoid kidney injury in a GM mouse model. In conclusion, SDAPR, SDAP1 and SDAP2 can be used to prevent GM-induced HEK293 cytotoxicity, probably because they have strong anti-oxidative stress, anti-inflammatory and anti-apoptotic effects. And SDAP1 and SDAP2 can inhibit GM-induced acute kidney injury in mice.

scholarly journals Obeticholic acid ameliorates hepatorenal syndrome in ascitic cirrhotic rats by down-regulating the renal 8-iso-PGF2α-activated COX-TXA2 pathway

2020 ◽  
Vol 134 (15) ◽  
pp. 2055-2073
Author(s):  
Yu-Lien Tsai ◽  
Chih-Wei Liu ◽  
Chien-Fu Hsu ◽  
Chia-Chang Huang ◽  
Ming-Wei Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatorenal Syndrome ◽  
Rat Kidney ◽  
Kidney Injury ◽  
Tubular Damage ◽  
Obeticholic Acid ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Duct Ligation ◽  
Renal Tubular

Abstract Backgrounds/Aims: The present study explores the potential of chronic treatment with the Foresaid X receptor (FXR) agonist obeticholic acid (OCA), which inhibits oxidative stress-related pathogenesis, in ascitic cirrhotic rats with hepatorenal syndrome (HRS) developed 6 weeks after bile duct ligation (BDL). Methods: Systemic, splanchnic, and renal hemodynamics and pathogenic cascades were measured in ascitic BDL and sham rats receiving 2-weeks of either vehicle or OCA treatments (sham-OCA and BDL-OCA groups), and NRK-52E cells, rat kidney tubular epithelial cells. Results: Chronic OCA treatment significantly normalized portal hypertension, glomerular filtration rate, urine output, renal blood flow; decreased ascites, renal vascular resistance, serum creatinine, and the release of renal tubular damage markers, including urinary neutrophil gelatinase-associated lipocalin (uNGAL) and kidney injury moleculae-1 (uKim-1) in BDL-OCA rats. In the BDL group, inhibition of the renal oxidative stress (8-iso-PGF2α)-activated cyclooxygenase-thromboxane A2 [COX-TXA2] pathway, apoptosis, and tubular injury accompanied by a decrease in hyper-responsiveness to the vasoconstrictor 8-iso-PGF2α in perfused kidneys. In vitro experiments revealed that 8-iso-PGF2α induced oxidative stress, release of reactive oxygen species, and cell apoptosis, which were reversed by concomitant incubation with the FXR agonist. Conclusions: Through the inhibition of renal 8-iso-PGF2α production and the down-regulation of the COX-TXA2 pathway, our study suggests that chronic OCA treatment can ameliorate the HRS in ascitic cirrhotic rats. Thus, OCA is an agent with antioxidative stress, antivasoconstrictive, antiapoptotic properties which benefit ascitic, cirrhotic rats with systemic, hepatic, and renal abnormalities.

Effect of Reynoutria Japonica and its Extract on Sirt1 in Cisplatin-Induced Renal Injury

2021 ◽  
Author(s):  
Shangmei Cao ◽  
Xiaojing Liu ◽  
Xinxin sun ◽  
Xixia Chen ◽  
Shuifu Tang
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Protein Expression ◽  
Kidney Injury ◽  
Model Group ◽  
Drug Induced ◽  
Blank Group ◽  
Reynoutria Japonica ◽  
Gene And Protein Expression ◽  
Sirt1 Gene

Abstract Background: Mechanisms of drug-induced kidney injury include mitochondrial dysfunction and oxidative stress. Resveratrol is a natural activator of sirt1 that is related to oxidative stress.Aim: To explore the mechanism of treating drug-induced kidney injury with Reynoutria japonica and its extract (Resveratrol).Design: Fifty adult male SD rats were randomly divided into five groups: blank group, model group, Reynoutria japonica group, resveratrol group and lotensin group. Each group was given the corresponding drug. ACR was measured on the seventh day every week. Creatinine and urea nitrogen were measured on the fourth weekend. All rats were sacrificed on the fourth weekend to detect the relevant indicators in the kidney.Results: At the fourth week, the ACR, Scr and BUN of the Resveratrol group were higher than those of the lotensin group and Reynoutria japonica group (P<0.05). The values of Scr and BUN were lower in the Reynoutria japonica group than in the lotensin group (P<0.05). The levels of SOD, NO, and sirt1 gene and protein expression in the model group and treatment group were lower than those in the blank group, and those in the model group were lower than those in the treatment group (P<0.05). The levels of SOD, NO, and sirt1 gene and protein expression in the Reynoutria japonica group were higher than the lotensin group (P<0.05).Conclusions: The therapeutic effect of the Reynoutria japonica group was better than that of the lotensin group and resveratrol group.

scholarly journals Effect of Reynoutria Japonic and Resveratrol on Sirt1/SOD/MDA of Adriamycin-Induced Renal Injury: A Randomised Trial

2021 ◽  
Author(s):  
Shangmei Cao ◽  
xiaojing liu ◽  
xinxin sun ◽  
xixia chen ◽  
shuifu Tang
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Injury ◽  
Group Model ◽  
Mrna Levels ◽  
Model Group ◽  
Drug Induced ◽  
Blank Group ◽  
Reynoutria Japonica ◽  
Comparison Results

Abstract Background: Mechanisms of drug-induced kidney injury include mitochondrial dysfunction and oxidative stress. Resveratrol is a natural activator of sirt1 that is related to oxidative stress.Objectives: To explore the mechanism of treating drug-induced kidney injury with Reynoutria japonica and its extract (Resveratrol).Methods: Fifty adult male SD rats were randomly divided into five groups: blank group, model group, Reynoutria japonica group, resveratrol group and Benazepril group. Except the blank group, each group used a one-time tail vein injection of 7.5mg/kg adriamycin to make the rat model of drug-induced renal injury. After three days, the proteinuria test strip showed green, which was positive for proteinuria. Each group was given the corresponding drug. ACR was measured on the seventh day every week. All rats were anaesthetized death on the fourth weekend to obtain blood and kidneys. Results: At the fourth week, the MDA levels of blank group and Reynoutria japonica group were significantly lower than those of benazepril hydrochloride group (P<0.05), and the MDA levels of resveratrol group and model group were significantly higher than those of benazepril hydrochloride group (P<0.05).The Sirt1 mRNA levels of the blank group and the Reynoutria japonica group were significantly higher than those in the benazepril hydrochloride group (P<0.05), and the Sirt1 mRNA levels of resveratrol group and model group were significantly lower than those of the benazepril hydrochloride group (P<0.05). The comparison results between groups of the Sirt1 protein expression were the same as those of the Sirt1 mRNA expression (P<0.05).Conclusions: The therapeutic effect of the Reynoutria japonica group was better than that of the Benazepril group and resveratrol group.

scholarly journals Renoprotective Effect of Formononetin against Cyclophosphamide-Induced Oxidative Stress and Inflammation in Rat Kidney

2021 ◽  
pp. 26-37
Author(s):  
Saleem H. Aladaileh ◽  
Farhan K. Al-Swailmi ◽  
Mohammad H. Abukhalil ◽  
Mohammed H. Shalayel
Keyword(s):  
Oxidative Stress ◽  
Single Injection ◽  
Biological Activities ◽  
Rat Kidney ◽  
Kidney Injury ◽  
Therapeutic Effects ◽  
Chemotherapy Agent ◽  
Apoptotic Protein ◽  
Protective Strategy ◽  
Pro Inflammatory Cytokines

Aims: Cyclophosphamide (CP) is a broad-spectrum chemotherapy agent available to treat various malignancies; however, its nephrotoxicity limits its clinical use. Formononetin (FOR) is a bioactive isoflavone with encouraging biological activities. The current study explored and elucidated the possible protective/therapeutic effects of formononetin against CP-induced nephrotoxicity. Methodology: Rats received FOR (40 mg/kg/day) for 15 days followed by a single injection of CP on day 16. CP-induced nephrotoxicity is characterized by an increase in urea and creatinine levels in serum. Kidney homogenate was used to assess MDA, NO and antioxidants. Results: CP-administered rats showed increased renal malondialdehyde and nitric oxide along with declined glutathione and antioxidant enzymes. In addition, CP increased pro-inflammatory cytokines and pro-apoptotic proteins levels and decreased anti-apoptotic protein Bcl2 levels in the kidney. FOR prevented CP-induced kidney injury, enhanced antioxidants and suppressed oxidative stress, pro-inflammatory mediators and apoptosis. Conclusion: These findings suggest that FOR prevents CP nephrotoxicity by attenuating the oxidative damage and inflammation. Therefore, our data suggest that FOR may represent a novel protective strategy against CP-induced nephrotoxicity, which deserves pursuit in further studies.

scholarly journals The protective effect of hesperidin against renal ischemia-reperfusion injury involves the TLR-4/NF-κB/iNOS pathway in rats

2020 ◽  
Vol 107 (1) ◽  
pp. 82-91 ◽  
Author(s):  
X. Meng ◽  
M. Wei ◽  
D. Wang ◽  
X. Qu ◽  
K. Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Group Treatment ◽  
Renal Injury ◽  
Ischemia Reperfusion Injury ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Altered Level ◽  
Mediators Of Inflammation

AbstractRenal injury is reported to have a high mortality rate. Additionally, there are several limitations to current conventional treatments that are used to manage it. This study evaluated the protective effect of hesperidin against ischemia/reperfusion (I/R)-induced kidney injury in rats. Renal injury was induced by generating I/R in kidney tissues. Rats were then treated with hesperidin at a dose of 10 or 20 mg/kg intravenously 1 day after surgery for a period of 14 days. The effect of hesperidin on renal function, serum mediators of inflammation, and levels of oxidative stress in renal tissues were observed in rat kidney tissues after I/R-induced kidney injury. Moreover, protein expression and mRNA expression in kidney tissues were determined using Western blotting and RT-PCR. Hematoxylin and eosin (H&E) staining was done for histopathological observation of kidney tissues. The data suggest that the levels of blood urea nitrogen (BUN) and creatinine in the serum of hesperidin-treated rats were lower than in the I/R group. Treatment with hesperidin also ameliorated the altered level of inflammatory mediators and oxidative stress in I/R-induced renal-injured rats. The expression of p-IκBα, caspase-3, NF-κB p65, Toll-like receptor 4 (TLR-4) protein, TLR-4 mRNA, and inducible nitric oxide synthase (iNOS) was significantly reduced in the renal tissues of hesperidin-treated rats. Histopathological findings also revealed that treatment with hesperidin attenuated the renal injury in I/R kidney-injured rats. In conclusion, our results suggest that hesperidin protects against renal injury induced by I/R by involving TLR-4/NF-κB/iNOS signaling.

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