• Toxicological Research
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• v.34 no.2
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• pp.143-150
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• 2018

It has been demonstrated that vanadate causes nephrotoxicity. Vanadate inhibits renal sodium potassium adenosine triphosphatase (Na, K-ATPase) activity and this is more pronounced in injured renal tissues. Cardiac cyclic adenosine monophosphate (cAMP) is enhanced by vanadate, while increased cAMP suppresses Na, K-ATPase action in renal tubular cells. There are no in vivo data collectively demonstrating the effect of vanadate on renal cAMP levels; on the abundance of the alpha 1 isoform (${\alpha}_1$) of the Na, K-ATPase protein or its cellular localization; or on renal tissue injury. In this study, rats received a normal saline solution or vanadate (5 mg/kg BW) by intraperitoneal injection for 10 days. Levels of vanadium, cAMP, and malondialdehyde (MDA), a marker of lipid peroxidation were measured in renal tissues. Protein abundance and the localization of renal ${\alpha}_1-Na$, K-ATPase was determined by Western blot and immunohistochemistry, respectively. Renal tissue injury was examined by histological evaluation and renal function was assessed by blood biochemical parameters. Rats treated with vanadate had markedly increased vanadium levels in their plasma, urine, and renal tissues. Vanadate significantly induced renal cAMP and MDA accumulation, whereas the protein level of ${\alpha}_1-Na$, K-ATPase was suppressed. Vanadate caused renal damage, azotemia, hypokalemia, and hypophosphatemia. Fractional excretions of all studied electrolytes were increased with vanadate administration. These in vivo findings demonstrate that vanadate might suppress renal ${\alpha}_1-Na$, K-ATPase protein functionally by enhancing cAMP and structurally by augmenting lipid peroxidation.

• The Journal of Internal Korean Medicine
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• v.26 no.2
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• pp.498-505
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• 2005

Renal failure means irreversible damage and depression of renal function, represented by glomerular filtration rate(GFR). A renal failure patient with uremia and anemia is presented. Anemia, in this patient, appeared before uremia did. A 55 year-old male patient was treated for renal failure with Weilingtang. Improvement was observed in, not only GFR, blood urea nitrogen(BUN), and creatinine, but also in such symptoms as difficulty in urine excretion, dyspepsia and abdominal swelling. But anemia appeared during treatment, so a mixture of Dangguibuxuetang(當歸補血湯) and Xiongguitang(芎歸湯) was prescribed. After this treatment, improvement in hemoglobin, and hematocrit was observed.

• Herbal Formula Science
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• v.31 no.3
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• pp.157-169
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• 2023

Gracilaria Verrucosa (GV), a seaweed used in traditional Korean medicine, was studied for its effects on MI-induced heart failure in rats. MI is caused by a blocked coronary artery, leading to severe cardiac dysfunction. The study used a rat model to assess cardiac changes over time and evaluate the impact of GV on heart failure. Ischemia was induced through LAD ligation surgery, and the extent of ischemic area was measured as a prognostic factor. GV extract administration significantly improved cardiac morphology and reduced cardiac weight compared to the MI group. GV treatment also improved cardiac function, as evidenced by positive effects on chamber dilation during MI-induced heart failure. Parameters such as ejection fraction (EF) and fractional shortening (FS) were measured. The MI group showed decreased EF and FS compared to the sham group, while these parameters improved in the GV group. GV treatment also reduced levels of LDH, CPK, and CK-MB in the serum, indicating reduced myocardial damage. Histological analysis revealed that GV treatment attenuated cardiac hypertrophy and fibrosis, with reduced collagen deposition in the myocardium. Immunohistochemistry analysis showed suppressed expression of TGF-β1 and collagen 1, involved in fibrosis. In conclusion, GV showed potential in improving cardiac function in a rat model of MI-induced heart failure. It alleviated myocardial damage, attenuated cardiac hypertrophy and fibrosis, and suppressed fibrotic markers. Further studies are needed to explore its clinical efficacy and underlying mechanisms in cardiac diseases beyond animal models.

• Nutrition Research and Practice
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• v.5 no.4
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• pp.365-369
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• 2011

This study investigated the preventive effect of Saururus chinensis Baill against renal damage induced by a high-fructose diet in rats. The rats (n = 30) were fed either a cornstarch-based (65%), high-fructose (65%), or high-fructose (64.5%) diet with 0.5% S. chinensis Baill extract for 10 weeks. Twenty-four hour urine collections were obtained and the animals were sacrificed after an overnight fast. Serum urea and creatinine and urine albumin were measured using colorimetric methods, and creatinine clearance was determined. In addition, thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), and the activity of superoxide dismutase (SOD) in the kidney were determined. Kidney samples were also examined histologically. The fructose-fed rats showed renal dysfunction, indicated by decreased creatinine clearance, increased albumin in the urine, and increased urea and creatinine in the serum. These renal function parameters were comparable to control levels in rats that consumed S. chinensis Baill. Fructose consumption increased renal TBARS and reduced GSH and SOD activity, whereas these levels were near-normal in the rats consuming S. chinensis Baill The kidneys of fructose-fed rats showed glomerular basement membrane thickening, mesangial matrix expansion, and tubule dilation. These pathological changes were not seen in the rats that consumed S. chinensis Baill. Therefore, S. chinensis Baill effectively alleviated fructose-induced renal damage in these rats, at least partially due to antioxidant activity.

• Journal of Chest Surgery
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• v.25 no.3
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• pp.232-239
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• 1992

Acute renal failure is a well known serious complication following open heart surgery and is associated with a significant increase in morbidity and mortality rate. From 1984 to 1990, 33 patients who had acute renal failure following cardiopulmonary bypass received renal replacement therapy. PD[Peritonial dialysis] was employed in 11 patients and CAVH[continous arteriovenous hemofiltration] was employed in 22 patients. Their age ranged from 3 months to 64 years[mean 25.5$\pm$7.8 years]. The disease entities included congenital cardiac anomaly in 18, valvular heart disease in 15 and aorta disease in 2 cases. Low cardiac output was thought as a primary cause of ARF except two redo valve cases who showed severe Aemolysis k depressed renal function preoperatively. Mean serum BUN and creatinine level at the onset renal replacement therapy were 65$\pm$8 mg/dl and 3.5$\pm$0.4 mg/dl respectively, declining only after reaching peak level 7&10 days following the onset of therapy. Overall hospital mortality was 72.7%[24/33]; 81%[9/11] in PD group and 68.2% [15/22] in CAVH group respectively. The primary cause of death was low cardiac output & hemodynamic depression in all the cases. The fatal complications included multiorgan failure in 7, disseminated intravascular coagulation and sepsis in 6, neurologic damage in 4 and mediastinitis in 3 cases. No measurable differences were observed between CAVH and PD group upon consequence of acute renal failure and disease per se. The age at operation, BUN/Cr level at the onset of bypass and highest BUN/Cr level and the consequence of low output status were regarded as important risk factors, determining outcome of ARF and success of renal replacement therapy. Thus, we concluded that althoght the prognosis is largely determined by severity of low cardiac output status and other organ complication, early institution of renal replacement therapy with other intensive supportive measures could improve salvage rate in established ARF patients following CPB.

• The Korea Journal of Herbology
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• v.28 no.3
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• pp.7-15
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• 2013

Objectives : Interruption and subsequent restoration of blood flow into the kidney result in renal injury. As an approach to preventing the renal injury, we determined the optimal conditions and the underlying mechanisms by which supernatant of hot water extract of ground Triticum aestivum L. (extract) attenuated ischemia/reperfusion (I/R) injury. Methods : One hour after administration of the extract (400 mg/kg) by intraperitoneal injection, renal I/R injury was generated by clamping the left renal artery in rats after surgical removal of the right kidney, followed by reperfusion. The maximal difference between the vehicle-treated and the extract-treated group under ketamine/xylazine or enflurane anesthetization was assessed at varying periods of ischemia (30-45 min) and reperfusion (3-48 hr), based on the renal function assessed with serum creatinine levels, tissue injury with hematoxylin/eosin staining, and apoptosis with terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling staining. Results : Enflurane anesthetization with 40 min of ischemia and 24 hr of reperfusion was identified to be the optimal condition, under which condition serum creatinine levels and tubular damage in the extract-treated group were significantly reduced compared with those in the vehicle-treated group ($1.3{\pm}0.2$ versus $2.7{\pm}0.3$ mg/dL, P < 0.01, and average score $1.8{\pm}0.1$ versus $3.5{\pm}0.3$, P < 0.01, respectively). These beneficial effects were mediated by inhibition of apoptotic cascades through attenuation of renal tissue malondialdehyde levels, Bax/Bcl-2 ratio and caspase-3 levels. Conclusions : The extract conferred renal protection against ischemia/reperfusion injury in rats by scavenging reactive oxygen species and consequently blocking apoptotic cascades, plausibly augmented by enflurane protection.

• Natural Product Sciences
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• v.28 no.4
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• pp.194-200
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• 2022

Albizia julibrissin Durazz. (AJ; family Minosaceae) is widely distributed worldwide, and its stem bark has been used as a traditional herbal medicine. Acute kidney injury (AKI) is a clinical syndrome that results in sudden loss of renal function. This study aimed to investigate the effects of AJ against cisplatin-induced AKI using a human kidney proximal tubule epithelial cell line (HK-2) and cisplatin-treated mice. In vitro, cisplatin treatment increased apoptosis in HK-2 cells. However, AJ treatment decreased apoptosis of cisplatin-treated HK-2 cells. In vivo, cisplatin treatment accelerated renal injury by increasing the levels of renal injury markers, such as blood urea nitrogen, creatinine, kidney injury molecule 1, and neutrophil gelatinase-associated lipocalin, which were reversed by AJ treatment. Histopathologically, AJ treatment resulted in decreased renal damage with less tubular necrosis and brush border desquamation compared with the AKI group. Additionally, cisplatin treatment upregulated mitochondrial fission, a pathological characteristic of AKI, which was downregulated by AJ treatment. Along with increased mitochondrial fission, AJ treatment also reduced cisplatin-induced apoptosis. These results suggest that AJ may be a potential therapeutic agent for cisplatin-induced AKI.

• Journal of Korean Medicine for Obesity Research
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• v.22 no.2
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• pp.167-172
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• 2022

Obesity is known as the most common risk factor for non-alcoholic fatty liver disease. Weight loss is needed to prevent liver function damage from progressing to non-alcoholic hepatosteatosis (NASH) and NASH-related liver cirrhosis. The purpose of this study was to observe the recovery of liver function in obese patients with liver dysfunction through traditional Korean obesity treatment. Body weight, liver function levels and renal function levels were examined by prescribing traditional Korean medicine in obese patients with mild elevation of liver function test. Blood tests were conducted at intervals of one month, and it was observed that liver function recovered to the normal range in three patients.

• Biomedical Science Letters
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• v.3 no.2
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• pp.151-160
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• 1997

This study was planned to evaluate the urinary ascorbic acid as a new biological marker for the intoxication of cadmium, which could possibly be driven by its increased utilization and environmental pollution. In order to meet this goal, we have peformed measurement of urinary ascorbic acid concentration, histopathological examination of the kidney, and biochemical test for the liver function using cadmium-intoxicated rats by oral administration. The average concentrations of urinary ascorbic acid in the $CdCl_2$-treated rats were 214.0 mg/dl for 100 ppm group and 254.3 mg/dl for 200 ppm group during experimental period of 50 days. These levels are 24 and 28 times higher than one in the control group (9.0 mg/dl), respectively. Ultrastructural study showed the eosinophilic hyaline cast and focal effacement, fusion in the renal tubules, as well as loss of foot processes on the glomerular epithelial cells. These results suggested that cadmium may be responsible for renal glomerular injury. The blood levels of AST, ALT and LDH in the treated groups (199 IU/I, 88 IU/I, 1190 U/I for the 100 ppm group and 270 IU/I, 226 IU/I, 760 U/I for the 200 ppm group) were higher than ones in the control group(143 IU/I, 50 IU/I, 334 U/I). These results indicated the cadmium induced the damage of liver function. In conclusion, the administration of cadmium showed a remarkable increase of urinary ascorbic acid with renal and hepatic damage. Therefore, it is expected that measurement of urinary ascorbic acid would be an powerful method as a noninvasive biomarker for cadmium intoxication.

• Journal of Veterinary Clinics
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• v.26 no.3
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• pp.200-204
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• 2009

This study was performed to evaluate the effects of reduced L-glutathione on the oxidant/antioxidant status(superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase(GPx), protein carbonyl and lipid hydroperoxide(LPO) concentration), renal function(blood urea nitrogen(BUN) and serum creatinine levels), and microscopy of renal tissues in pigs undergoing unilateral renal ischemia-reperfusion(I/R). Sixteen Landrace and Yorkshire mixed-breed pigs were divided randomly into two groups: untreated control group and reduced L-glutathione-treated group(4 mg/kg IV). Each group had 8 pigs. Pigs were unilaterally nephrectomized and the kidney was subject to 30 min of renal pedicle occlusion. Blood samples for biochemical assay were collected on days 1, 3, 5, 7, and 14 post nephrectomy. Renal I/R injury were evaluated histopathologically by the microscopic observation of renal tissue sections and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as SOD, GPx, CAT, protein carbonyl and LPO were measured. The elevation of creatine and BUN levels was lower in the treated group, compared with the control group. The activities of antioxidant-enzyme were higher in the treated group, compared with the control group. In histological findings, the severity of damage in the reduced L-glutathione treated group was less when compared to the control group.