scholarly journals Protective Effects of Ophiocordyceps lanpingensis on Glycerol-Induced Acute Renal Failure in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Yanyan Zhang ◽  
Yaxi Du ◽  
Hong Yu ◽  
Yongchun Zhou ◽  
Feng Ge
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Low Dose ◽  
Treated Group ◽  
High Dose ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Immune Organ

Objective. Oxidative stress and immune response are associated with acute renal failure (ARF). Ophiocordyceps lanpingensis (OL) might be an antioxidant and immunopotentiator. In this study, we explored the protective effects of OL on glycerol-induced ARF. Methods. Male mice were randomly divided into four groups, specifically, glycerol-induced ARF model group, low-dose OL-treated group (1.0 g/kg/d), high-dose OL-treated group (2.0 g/kg/d), and control group. Renal conditions were evaluated using kidney index, serum creatinine (Cr), blood urea nitrogen (BUN), and histological analysis. Rhabdomyolysis was monitored using creatine kinase (CK) level. Oxidative stress was determined using kidney tissue glutathione (GSH), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. Immune status was evaluated using immune organ indices and immunoglobulin G (IgG) level. Results. OL could relieve renal pathological injury and decrease the abnormal levels of kidney index, serum Cr, CK, BUN, and MDA, as well as increase the immune organ indices and the levels of IgG, GSH, and SOD. Treatment with a high dose of OL had more positive therapeutic effects on ARF than using a low dose of OL. Conclusion. OL could ameliorate renal dysfunction in glycerol-induced ARF in mice by inhibiting oxidative stress and enhancing immune response.

Proteomics ofS-(1, 2-dichlorovinyl)-l-cysteine-induced acute renal failure and autoprotection in mice

2007 ◽  
Vol 293 (4) ◽  
pp. F994-F1006 ◽  
Author(s):  
Midhun C. Korrapati ◽  
Jaya Chilakapati ◽  
Frank A. Witzmann ◽  
Chundury Rao ◽  
Edward A. Lock ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Low Dose ◽  
Lethal Dose ◽  
High Dose ◽  
Two Dimensional Gel Electrophoresis ◽  
Α Subunit ◽  
Treatment Groups ◽  
Liquid Chromatography Tandem Mass

Previous studies (Vaidya VS, Shankar K, Lock EA, Bucci TJ, Mehendale HM. Toxicol Sci 74: 215–227, 2003; Korrapati MC, Lock EA, Mehendale HM. Am J Physiol Renal Physiol 289: F175–F185, 2005; Korrapati MC, Chilakapati J, Lock EA, Latendresse JR, Warbritton A, Mehendale HM. Am J Physiol Renal Physiol 291: F439–F455, 2006) demonstrated that renal repair stimulated by a low dose of S-(1,2-dichlorovinyl)l-cysteine (DCVC; 15 mg/kg ip) 72 h before administration of a normally lethal dose (75 mg/kg ip) protects mice from acute renal failure (ARF) and death (autoprotection). The present study identified the proteins indicative of DCVC-induced ARF and autoprotection in male Swiss Webster mice. Renal dysfunction and injury were assessed by plasma creatinine and histopathology, respectively. Whole-kidney homogenates were run on two-dimensional gel electrophoresis gels, and the expression of 18 common proteins was maximally changed (≥10-fold) in all the treatment groups and they were conclusively identified by liquid chromatography tandem mass spectrometry. These proteins were mildly downregulated after low dose alone and in autoprotected mice in contrast to severe downregulation with high dose alone. Glucose-regulated protein 75 and proteasome α-subunit type 1 were further investigated by immunohistochemistry for their localization in the kidneys of all the groups. These proteins were substantially higher in the proximal convoluted tubular epithelial cells in the low-dose and autoprotected groups compared with high-dose alone group. Proteins involved in energetics were downregulated in all the three groups of mice, leading to a compromise in cellular energy. However, energy is recovered completely in low-dose and autoprotected mice. This study provides the first report on proteomics of DCVC-induced ARF and autoprotection in mice and reflects the application of proteomics in mechanistic studies as well as biomarker development in a variety of toxicological paradigms.

scholarly journals Amniotic fluid stem cells ameliorate cisplatin-induced acute renal failure through induction of autophagy and inhibition of apoptosis

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ekta Minocha ◽  
Rohit Anthony Sinha ◽  
Manali Jain ◽  
Chandra Prakash Chaturvedi ◽  
Soniya Nityanand
Keyword(s):  
Stem Cells ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Amniotic Fluid ◽  
Cell Types ◽  
Treated Group ◽  
Protective Role ◽  
Protective Effects ◽  
Amniotic Fluid Stem Cells

Abstract Background We have recently demonstrated that amniotic fluid stem cells (AFSC) express renal progenitor markers and can be differentiated in vitro into renal lineage cell types, viz, juxtaglomerular and renal proximal tubular epithelial-like cells. Here, we have evaluated the therapeutic efficacy of AFSC in a cisplatin-induced rat model of acute renal failure (ARF) and investigated the underlying mechanisms responsible for their renoprotective effects. Methods ARF was induced in Wistar rats by intra-peritoneal injection of cisplatin (7 mg/kg). Five days after cisplatin injection, rats were randomized into two groups and injected with either AFSC or normal saline intravenously. On days 8 and 12 after cisplatin injection, the blood biochemical parameters, histopathological changes, apoptosis and expression of pro-apoptotic, anti-apoptotic, and autophagy-related proteins in renal tissues were studied in both groups of rats. To further confirm whether the protective effects of AFSC on cisplatin-induced apoptosis were dependent on autophagy, chloroquine, an autophagy inhibitor, was administered by the intra-peritoneal route. Results Administration of AFSC in ARF rats resulted in improvement of renal function and attenuation of renal damage as reflected by significant decrease in blood urea nitrogen, serum creatinine levels, tubular cell apoptosis as assessed by Bax/Bcl2 ratio, and expression of the pro-apoptotic proteins, viz, PUMA, Bax, cleaved caspase-3, and cleaved caspase-9, as compared to the saline-treated group. Furthermore, in the AFSC-treated group as compared to the saline-treated group, there was a significant increase in the activation of autophagy as evident by increased expression of LC3-II, ATG5, ATG7, Beclin1, and phospho-AMPK levels with a concomitant decrease in phospho-p70S6K and p62 expression levels. Chloroquine administration led to significant reduction in the anti-apoptotic effects of the AFSC therapy and further deterioration in the renal structure and function caused by cisplatin. Conclusion AFSC led to amelioration of cisplatin-induced ARF which was mediated by inhibition of apoptosis and activation of autophagy. The protective effects of AFSC were blunted by chloroquine, an inhibitor of autophagy, highlighting that activation of autophagy is an important mechanism of action for the protective role of AFSC in cisplatin-induced renal injury.

Molecular mechanisms of enhanced renal cell division in protection against S-1,2-dichlorovinyl-l-cysteine-induced acute renal failure and death

2005 ◽  
Vol 289 (1) ◽  
pp. F175-F185 ◽  
Author(s):  
Midhun C. Korrapati ◽  
Edward A. Lock ◽  
Harihara M. Mehendale
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Cell Division ◽  
Cyclin D1 ◽  
Renal Cell ◽  
Low Dose ◽  
Lethal Dose ◽  
S Phase ◽  
High Dose ◽  
Priming Dose

Sustained activation of ERK 1/2 by a low dose (15 mg/kg ip) of S-1,2-dichlorovinyl-l-cysteine (DCVC) 72 h before administration of a lethal dose of DCVC (75 mg/kg ip) enhances renal cell division and protects mice against acute renal failure (ARF) and death (autoprotection). The objective of this study was to determine correlation among extent of S-phase DNA synthesis, activation of transcription factors, expression of G1/S cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors downstream of ERK 1/2 following DCVC-induced ARF in autoprotection. Administration of the lethal dose alone caused a general downregulation or an unsustainable increase, in transcriptional and posttranscriptional events thereby preventing G1-S transition of renal cell cycle. Phosphorylation of IκBα was inhibited resulting in limited nuclear translocation of NF-κB. However, cyclin D1 expression was high probably due to transcriptional cooperation of AP-1. Cyclin D1/cyclin-dependent kinase 4 (cdk4)-cdk6 system-mediated phosphorylation of retinoblastoma protein was downregulated due to overexpression of p16 at 24 h after exposure to the lethal dose alone. Inhibition of S-phase stimulation was confirmed by proliferating cell nuclear antigen assay (PCNA). This inhibitory response was prevented if the lethal dose was administered 72 h after the low priming dose of DCVC due to promitogenic effect of the low dose. NF-κB-DNA binding is not limited if mice were pretreated with the priming dose. Cyclin D1/cdk4-cdk6 expression stimulated by the priming dose of DCVC was unaltered even after the lethal dose in the autoprotected group, explaining higher phosphorylated-pRB and S-phase stimulation found in this group. These results were corroborated with PCNA immunohistochemistry. These findings suggest that the priming dose relieves the block on compensatory tissue repair by upregulation of promitogenic mechanisms, normally blocked by the high dose when administered without the prior priming dose.

scholarly journals Protective Effect of Ginsenoside Against Acute Renal Failure via Reduction of Renal Oxidative Stress and Enhanced Expression of ChAT in the Proximal Convoluted Tubule and ERK1/2 in the Paraventricular Nuclei

2014 ◽  
pp. 597-604 ◽  
Author(s):  
J. ZHOU ◽  
H. A. ZHANG ◽  
Y. LIN ◽  
H. M. LIU ◽  
Y. M. CUI ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
Protective Effects ◽  
Paraventricular Nuclei ◽  
Mitogen Activated Protein ◽  
Enhanced Expression ◽  
Mapk Signal Pathway ◽  
Hypothalamic Paraventricular Nuclei

Generation of reactive oxygen species significantly contributes to the pathogenesis of acute renal failure (ARF) induced by myoglobin release. Ginsenosides (GS), the principal active ingredients of ginseng, is considered as an extremely good antioxidative composition of Chinese traditional and herbal drugs. The purpose of the present study was to investigate the protective effect of ginsenoside in rats with ARF on the changes of cholinergic nervous system in the kidney as well as on the involvement of mitogen-activated protein kinases (MAPK) in the hypothalamic paraventricular nuclei (PVN). In our assay, glycerol-induced acute renal failure in rats was employed to study the protective effects of ginsenoside. Our results indicated that the treatment of ARF rats with ginsenosides for 48 h significantly reduced lipid peroxidation, restored the superoxide dismutase (SOD) level. Meanwhile, the obvious increase of choline acetyltransferase-immunoreactivity (ChAT-IR) in the proximal convoluted tubular cells (PCT) was observed by immunohistochemistry in ARF+GS group. The same effect was also observed in the changes of p-ERK1/2-IR in the hypothalamic paraventricular nuclei. Our results suggest that ginsenoside administered orally may have a strong renal protective effect against glycerol-induced ARF, reduce the renal oxidative stress, and ginsenoside can also activate the cholinergic system in PCT, simultaneously MAPK signal pathway in the PVN was also activated.

scholarly journals The Protective Effects of Cobra Venom fromNaja naja atraon Acute and Chronic Nephropathy

2013 ◽  
Vol 2013 ◽  
pp. 1-17 ◽  
Author(s):  
Shu-Zhi Wang ◽  
He He ◽  
Rong Han ◽  
Jia-Li Zhu ◽  
Jian-Qun Kou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Kidney Diseases ◽  
Therapeutic Drug ◽  
Protective Effects ◽  
Protein Determination ◽  
Chronic Nephropathy ◽  
Transmission Electron ◽  
Glycerol Injection

This study investigated the effects ofNaja naja atravenom (NNAV) on acute and chronic nephropathy in rats. Rats received 6 mg/kg adriamycin (ADR) once to evoke the chronic nephropathy or 8 ml/kg 50% v/v glycerol to produce acute renal failure (ARF). The NNAV was given orally once a day starting five days prior to ADR or glycerol injection and continued to the end of experiments. The animals were placed in metabolic cages for 24 h for urine collection for urinary protein determination. The kidney function-related biochemical changes and index of oxidative stress were determined with automatic biochemistry analyzer or colorimetric enzyme assay kits. The pathomorphological changes were observed using light and transmission electron microcopies. The levels of inflammatory cytokines and NF-κB activation were determined using ELISA kits, Western blot analysis, or immunofluorescence. The results showed that NNAV relieved ADR-induced chronic nephropathy and glycerol-triggered acute renal failure syndromes including proteinuria, hypoalbuminemia, hyperlipidemia, serum electrolyte unbalance, renal oxidative stress, and pathological damages. NNAV reduced kidney levels of TNF-αand IL-1β, but it increased the levels of IκB-αand inhibited NF-κB p65 nuclear localization. These findings suggest that NNAV may be a valuable therapeutic drug for acute and chronic kidney diseases.

Protective Effects of Flavonoids from Lotus Leaf against Exercise-Induced Oxidant Stress in Muscle of Mice

2013 ◽  
Vol 448-453 ◽  
pp. 1089-1092 ◽  
Author(s):  
Lan Zhang
Keyword(s):  
Low Dose ◽  
Oxidant Stress ◽  
Treated Group ◽  
Control Group ◽  
High Dose ◽  
Protective Effects ◽  
Lotus Leaf ◽  
Swimming Time ◽  
Exercise Induced ◽  
Different Doses

The main purpose of this study was to examine the effect of flavonoids from Lotus leaf (FFL) on exercise-induced oxidant stress in mice. 32 mice were randomly divided into 4 groups: control group, FLL low dose treated group, FLL middle dose treated group and FLL high dose treated group. The control group was given distilled water and the treated groups were given different doses of FLL (50, 100, 150 mg/kg) by gavage once a day for 28 days. 28 day later, mice were made to swim until being exhausted, and exhaustive swimming time, malondialdehyde (MDA) levels, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in muscle were measured. The data showed that that FFL increase the exhaustive swimming time and could elevate the exercise tolerance, as well as decrease the MDA levels, increase SOD and GSH-Px activities in muscle of mice. These results indicated that FFL has a protective effect against exercise-induced oxidative stress.

L-Citrulline Protects against Rhabdomyolysis -Induced Acute Renal Failure in Rats

2013 ◽  
Vol 634-638 ◽  
pp. 1323-1327
Author(s):  
Xiao Bin Fu ◽  
Sai Li ◽  
Li Liu ◽  
Ling Shan Gou ◽  
Nuo Lan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Nitric Oxide Synthase ◽  
Protective Effects ◽  
Renal Deterioration ◽  
Stress Damage ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

There is increasing evidence indicating that oxidative stress plays an important role in the pathogenesis of rhabdomyolysis-induced myoglobinuric acute renal failure (ARF). In this study, protective effects of L-citrulline on glycerol-induced acute renal failure (ARF) in rats were investigated. Six groups of rats were employed in this study, after seven days of glycerol injections, the blood samples and kiney tissues were harvested for future biochemical and pathology analysis. The levels of creatinine (Cr) and urea nitrogen (BUN) in plasma, the content of malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO), the activity of total nitric oxide synthase (TNOS), inducible nitric oxide synthase (iNOS), endothelial NO synthase (eNOS) and superoxide dismutase (SOD) were evaluated in kiney tissues. Consequently, treatment with L-citrulline improved an impaired intrarenal oxygenation and kidney function compare with the glycerol group, and prevented the renal oxidative stress damage as well as severe functional and morphological renal deterioration.

Effects of quercetin on cadmium-induced toxicity in rat urine using metabonomics techniques

2019 ◽  
Vol 39 (4) ◽  
pp. 524-536
Author(s):  
Y Liu ◽  
X Zhang ◽  
T Guan ◽  
S Jia ◽  
Y Liu ◽  
...  
Keyword(s):  
Low Dose ◽  
Treated Group ◽  
Urine Samples ◽  
Control Group ◽  
High Dose ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Rat Urine ◽  
Antioxidant Defence System ◽  
Liver And Kidney

This study aimed to analyse the protective effects of quercetin on the toxicity of cadmium (Cd) using metabonomics techniques. Sixty male Sprague–Dawley rats were randomly divided into six groups ( n = 10): control group (C), low-dose quercetin-treated group (Q1; 10 mg/kg bw/day), high-dose quercetin-treated group (Q2; 50 mg/kg bw/day), Cd-treated group (D; 4.89 mg/kg bw/day), low-dose quercetin plus Cd-treated group (DQ1) and high-dose quercetin plus Cd-treated group (DQ2). The rats continuously received quercetin and Cd via gavage and drinking water for 12 weeks, respectively. The rat urine samples were collected for metabonomics analysis. Finally, 10 metabolites were identified via the metabonomics profiles of the rat urine samples. Compared with the control group, the intensities of taurine, phosphocreatine, l-carnitine and uric acid were significantly decreased ( p < 0.01) and those of LysoPC (18: 2 (9Z, 12Z)), guanidinosuccinic acid, dopamine, 2,5,7,8-tetramethyl-2(2′-carboxyethyl)-6-hydroxychroman and allantoic acid were significantly increased ( p < 0.01) in the Cd-treated group. However, the intensities of the aforementioned metabolites had restorative changes in the high-dose quercetin plus Cd-treated groups unlike those in Cd-treated group ( p < 0.01 or p < 0.05). Results indicated that quercetin exerts protective effects on Cd-induced toxicity by regulating energy and lipid metabolism, enhancing the antioxidant defence system and protecting liver and kidney function and so on.

Effects of Polysaccharides from Radix astragali on Oxidative Stress Induced by Exhaustive Swimming Exercise in Liver and Muscle of Mice

2014 ◽  
Vol 633-634 ◽  
pp. 558-561
Author(s):  
Ming Wu ◽  
Dan Han ◽  
Chuan Fu Ma ◽  
Zhen Wei Wei ◽  
Jun Hong Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treated Group ◽  
Swimming Exercise ◽  
Control Group ◽  
High Dose ◽  
Protective Effects ◽  
Radix Astragali ◽  
Final Treatment ◽  
Exercise Induced ◽  
Different Doses

Polysaccharides, the mainly bioactive ingredient ofRadix Astragali, were evaluated for its effects on the oxidative stress induced by exhaustive swimming exercise of mice. A total of 48 mice were randomly divided into four groups: control group, low-dose polysaccharide fromAstragali radix(RAP) treated group, medium-dose RAP treated group, and high-dose RAP treated group. The control group received only distilled water ig, and the RAP treated groups received different doses of RAP (50, 100, and 200 mg/kg, ig) for 28 days. After the final treatment with RAP, the mice were subjected to swimming to exhaustion and the superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) were measured. The data showed that RAP promote increases in the activities of SOD, GPX and CAT in liver and muscle of mice, and the high-dose RAP (200 mg/kg) presented the best effect. These results indicated that RAP possessed protective effects against exercise-induced oxidative stress.

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