scholarly journals Protective Effect of Ginsenoside against Acute Renal Failure and Expression of Tyrosine Hydroxylase in the Locus Coeruleus

2010 ◽  
pp. 61-70 ◽  
Author(s):  
H A Zhang ◽  
M Wang ◽  
J Zhou ◽  
Q Y Yao ◽  
J M Ma ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Tyrosine Hydroxylase ◽  
Protective Effect ◽  
Locus Coeruleus ◽  
Great Effort ◽  
Protective Effects ◽  
Tubular Necrosis ◽  
Mitogen Activated Protein ◽  
Serum Blood Urea Nitrogen

Acute renal failure (ARF) is mainly characterized by acute tubular necrosis. No significant change was found for mortality rates over the past few decades despite significant advances in supportive care. In recent years, great effort has been focused on traditional and herbal medicine, which is much less toxic than those agents conventionally used and which is nowadays considered as a novel therapeutic agent for ARF. However, the effect of ginsenosides (GS) administered orally on ARF has not been reported yet and little is known about its cellular and molecular mechanism. The purpose of the study is to investigate the protective effect of ginsenoside in rats with ARF on the changes of tyrosine hydroxylase immunoreactivity (TH-IR) as well as on the involvement of mitogen-activated protein kinases (MAPK) in the locus coeruleus. 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 the serum blood urea nitrogen, creatinine level, and lipid peroxidation, restored the GSH level and the normal renal morphology. Immunohistochemistry showed that an obvious increase of TH-IR was further enhanced in ARF+GS group. The same effect was also observed in the changes of p-ERK1/2-IR in the locus coeruleus. Our results suggest that ginsenoside administered orally may have a strong renal protective effect against glycerol-induced ARF, and ginsenoside can also activate the brain catecholaminergic neurons in the locus coeruleus. Our future attention will be focused to the question whether there is a correlation between the renal protective effect of ginsenosides against acute renal failure and the activation of tyrosine hydroxylase in the locus coeruleus.

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 HPLC-PDA Simultaneous Determination and Protective Effect of Anemarrhena asphodeloides Against Acute Renal Failure

2014 ◽  
Vol 9 (6) ◽  
pp. 1934578X1400900
Author(s):  
Chang-Seob Seo ◽  
Hyekyung Ha ◽  
Young-Jung Kim ◽  
Ju-Young Jung
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Acetic Acid ◽  
Protective Effect ◽  
High Performance ◽  
Glutathione Depletion ◽  
Aqueous Acetic Acid ◽  
Protective Effects ◽  
Relative Standard ◽  
Anemarrhena Asphodeloides

We investigated the protective effects against acute renal failure (ARF) of Anemarrhena asphodeloides (AA) and performed simultaneous analysis of three compounds, neomangiferin (1), mangiferin (2), and isomangiferin (3) in AA using a high-performance liquid chromatography-photodiode array. To measure the protective effect of ARF, the levels of reactive oxygen species (ROS) and glutathione depletion were determined using a kit. HPLC analysis was performed using a Gemini C18 column at 40°C. The mobile phase used gradient elution with 1.0% (v/v) aqueous acetic acid (A) and 1.0% (v/v) acetic acid in acetonitrile (B). The flow rate was 1.0 mL/min. In our assay, AA extract inhibits cisplatin-induced production of intracellular ROS. Pre-incubation of AA extracts (10–200 μg/mL) markedly maintained cell viability compared with controls in the noncisplatin-treated cells. Calibration curves of all compounds showed good linearity ( r2  0.9992). Recoveries of the three compounds were 98.9–103.4%. The relative standard deviations of intra- and inter-day precision were 0.07–1.73% and 0.12–1.49%, respectively. The amounts of the three components were 1.22–20.63 mg/g. The AA extract has potential as a therapeutic agent for treatment of ARF. In addition, the established method will help to improve quality control of AA.

Oestrogen protects against ischaemic acute renal failure in rats by suppressing renal endothelin-1 overproduction

2002 ◽  
Vol 103 (s2002) ◽  
pp. 434S-437S ◽  
Author(s):  
Masanori TAKAOKA ◽  
Mikihiro YUBA ◽  
Toshihide FUJII ◽  
Mamoru OHKITA ◽  
Yasuo MATSUMURA
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Renal Dysfunction ◽  
Tissue Injury ◽  
Male Rats ◽  
Left Renal Artery ◽  
Protective Effects ◽  
Endothelin 1 ◽  
Ischaemia Reperfusion

We investigated whether the treatment with 17β-oestradiol has renal protective effects in male rats with ischaemic acute renal failure (ARF). We also examined if the effect of 17β-oestradiol is accompanied by suppression of enhanced endothelin-1 production in postischaemic kidneys. Ischaemic ARF was induced by clamping the left renal artery and vein for 45min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function parameters such as blood urea nitrogen, plasma creatinine and creatinine clearance were measured to test the effectiveness of the steroid hormone. Renal function in ARF rats markedly decreased 24h after reperfusion. The ischaemia/reperfusion-induced renal dysfunction was dose-dependently improved by pretreatment with 17β-oestradiol (20 or 100µg/kg, intravenously). Histopathological examination of the kidney of untreated ARF rats revealed severe lesions, such as tubular necrosis, proteinaceous casts in tubuli and medullary congestion, all of which were markedly improved by the higher dose of 17β-oestradiol. In addition, endothelin-1 content in the kidney after the ischaemia/reperfusion increased significantly by approx. 2-fold over sham-operated rats, and this elevation was dose-dependently suppressed by the 17β-oestradiol treatment. These results suggest that oestrogen exhibits protective effects against renal dysfunction and tissue injury induced by ischaemia/reperfusion, possibly through the suppression of endothelin-1 overproduction in postischaemic kidneys.

Evidence suggesting a role for hydroxyl radical in glycerol-induced acute renal failure

1988 ◽  
Vol 255 (3) ◽  
pp. F438-F443 ◽  
Author(s):  
S. V. Shah ◽  
P. D. Walker
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Hydroxyl Radical ◽  
Tissue Injury ◽  
Iron Chelator ◽  
Radical Scavenger ◽  
Reactive Oxygen Metabolites ◽  
Protective Effects ◽  
Hydroxyl Radical Scavenger ◽  
Hydroxyl Radical Scavengers

Reactive oxygen metabolites, in particular hydroxyl radical, have been shown to be important mediators of tissue injury in several models of acute renal failure. The aim of the present study was to examine the role of hydroxyl radical in glycerol-induced acute renal failure, a model for myoglobinuric renal injury. Rats injected with glycerol alone (8 mg/kg im following dehydration for 24 h) developed significant renal failure compared with dehydrated controls. Rats treated with glycerol and a hydroxyl radical scavenger, dimethylthiourea (DMTU), had significantly lower blood urea nitrogen (BUN) and creatinine. In contrast, urea, which is chemically similar to DMTU but is not a hydroxyl radical scavenger, provided no protection. In addition, DMTU prevented the glycerol-induced rise in renal cortical malondialdehyde content (a measure of lipid peroxidation that serves as a marker of free radical-mediated tissue injury). A second hydroxyl radical scavenger, sodium benzoate, had a similar protective effect on renal function (as measured by both BUN and creatinine). Because the generation of hydroxyl radical in biological systems requires the presence of a trace metal such as iron, we also examined the effect of the iron chelator, deferoxamine on glycerol-induced renal failure. Deferoxamine was also protective. The interventional agents were also associated with a marked reduction in histological evidence of renal damage. The protective effects of two hydroxyl radical scavengers as well as an iron chelator implicate a role for hydroxyl radical in glycerol-induced acute renal failure.

scholarly journals Renal involvement in human rabies: clinical manifestations and autopsy findings of nine cases from northeast of Brazil

2005 ◽  
Vol 47 (6) ◽  
pp. 315-320 ◽  
Author(s):  
Elizabeth De Francesco Daher ◽  
Geraldo Bezerra da Silva Júnior ◽  
Marúsia Thomaz Ferreira ◽  
Fernando Antonio de Sousa Barros ◽  
Tiago Magalhães Gurgel ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Involvement ◽  
Clinical Manifestations ◽  
Signs And Symptoms ◽  
Hemodynamic Instability ◽  
Human Rabies ◽  
Tubular Necrosis ◽  
Post Mortem Findings ◽  
Histopathologic Findings

A retrospective study was conducted in nine patients with rabies admitted to a hospital of Fortaleza, Brazil. Autopsy was performed in all cases. The ages ranged from three to 81 years and six were males. They all were bitten by dogs. The time between the accident and the hospital admission ranged from 20 to 120 days (mean 45 ± 34 days). The time until death ranged from one to nine days (mean 3.3 ± 5.5 days). The signs and symptoms presented were fever, hydrophobia, aerophobia, agitation, disorientation, dyspnea, sialorrhea, vomiting, oliguria, sore throat, pain and hypoesthesia in the site of the bite, headache, syncope, cough, hematemesis, mydriasis, hematuria, constipation, cervical pain and priapism. In three out of six patients, there was evidence of acute renal failure, defined as serum creatinine > 1.4 mg/dL. The post-mortem findings in the kidneys were mild to moderate glomerular congestion and mild to intense peritubular capillary congestion. Acute tubular necrosis was seen in only two cases. This study shows some evidence of renal involvement in rabies. Histopathologic findings are nonspecific, so hemodynamic instability, caused by autonomic dysfunction, hydrophobia and dehydration must be responsible for acute renal failure in rabies.

scholarly journals An evaluation of antioxidant effects on recovery from postischemic acute renal failure.

1994 ◽  
Vol 4 (8) ◽  
pp. 1588-1597
Author(s):  
R A Zager ◽  
S M Fuerstenberg ◽  
P H Baehr ◽  
D Myerson ◽  
B Torok-Storb
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Dna Fragmentation ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tubular Necrosis ◽  
Proliferating Cell

Xanthine oxidase (XO) activity and hydroxyl radical (.OH) formation are widely proposed mediators of renal reperfusion injury, potentially altering the severity of, and recovery from, postischemic acute renal failure. The goal of this study was to ascertain whether combination XO inhibitor (oxypurinol) and .OH scavenger (Na benzoate) therapy, given at the time of renal ischemia, alters the extent of: (1) tubular necrosis and filtration failure; (2) DNA fragmentation/apoptosis (assessed in situ by terminal deoxynucleotidyl transferase reactivity); (3) early tubular regenerative responses (proliferating cell nuclear antigen expression; (3H)thymidine incorporation); and (4) the rate and/or degree of functional and morphologic repair. The effects of XO inhibition, .OH scavengers, and "catalytic" iron (FeSO4) on human proximal tubular cell proliferation in vitro were also assessed with a newly established cell line (HK-2). Male Sprague-Dawley rats were subjected to 35 min of bilateral renal arterial occlusion with or without oxypurinol/benzoate therapy. These agents did not alter the extent of tubular necrosis or filtration failure, proliferating cell nuclear antigen expression or thymidine incorporation, or the rate/extent of renal functional/morphologic repair. DNA fragmentation did not precede tubular necrosis, and it was unaffected by antioxidant therapy. By 5 days postischemia, both treatment groups demonstrated regenerating epithelial fronds that protruded into the lumina. These structures contained terminal deoxynucleotidyl transferase-reactive, but morphologically intact, cells, suggesting the presence of apoptosis. Oxypurinol and .OH scavengers (benzoate; dimethylthiourea) suppressed in vitro tubular cell proliferation; conversely, catalytic Fe had a growth-stimulatory effect. These results suggest that: (1) XO inhibition/.OH scavenger therapy has no discernible net effect on postischemic acute renal failure; (2) DNA fragmentation does not precede tubular necrosis, suggesting that it is not a primary mediator of ischemic cell death; and (3) antioxidants can be antiproliferative for human tubular cells, possibly mitigating their potential beneficial effects.

scholarly journals Acute Renal Failure in a Tertiary Care Center in Nepal

2005 ◽  
Vol 44 (158) ◽  
Author(s):  
Sudha Khakurel ◽  
P R Satyal ◽  
R K Agrawal ◽  
P K Chhetri ◽  
R Hada
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Bacillary Dysentery ◽  
Care Center ◽  
Tertiary Care ◽  
Acute Interstitial Nephritis ◽  
Female Age ◽  
Tubular Necrosis ◽  
Common Causes ◽  
Urate Nephropathy

From July 1998 to July 1999, 45 cases of acute renal failure were treated at Bir Hospital, Kathmandu. Outof which 24 were male and 21 were female. Age ranged from 11 months to 84 years with mean age being 35years and 9 cases were below 10 years.Four cases with pre-renal azotaemia and twenty five cases of acute tubular necrosis (ATN) accounted for64% of all cases. These were due to gastroenteritis 10, sepsis 6, post surgical 1, trauma 1 and obstreticalcomplications 5. Multiple hornet stings were responsible for acute renal failure in 3 cases, acute urate nephropathy in 1 case and miscellaneous causes in 2 cases.Glomerulonephritis / vasculitis accounted for 17.7%, acute interstitial nephritis 4.4%, haemotytic uraemicsyndrome (HUS) 6.6%, and post renal azotaemia in 6.6% of all cases. Mean serum creatinine was 8 mg/dl,mean blood urea 190 mg/dl. Eight cases were treated only conservatively, eighteen received haemodialysis,fourteen received peritoneal dialysis, three received both and two refused for dialysis. Average duration ofhospital stay was 13.6 days. Out of the forty-five cases twenty-nine recovered normal renal function, tenexpired, two recovered partially, two progressed to chronic renal failure and two left against medical advice.Overall mortality was 22.2%.Common causes of acute renal failure in our setting were gastroenteritis (22%) and sepsis (20%). HUS wasexclusively seen in children following bacillary dysentery. Multiple hornet stings is an important cause ofacute renal failure in our country.

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