scholarly journals Cinnabar-Induced Subchronic Renal Injury Is Associated with Increased Apoptosis in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ying Wang ◽  
Dapeng Wang ◽  
Jie Wu ◽  
Bohan Wang ◽  
Xianhui Gao ◽  
...  
Keyword(s):  
Renal Injury ◽  
Death Receptor ◽  
Kidney Injury ◽  
Inflammatory Cells ◽  
Underlying Mechanism ◽  
Treated Group ◽  
Control Group ◽  
Antibody Array ◽  
Tubular Cells ◽  
Kidney Injury Molecule 1

The aim of this study was to explore the role of apoptosis in cinnabar-induced renal injury in rats. To test this role, rats were dosed orally with cinnabar (1 g/kg/day) for 8 weeks or 12 weeks, and the control rats were treated with 5% carboxymethylcellulose solution. Levels of urinary mercury (UHg), renal mercury (RHg), serum creatinine (SCr), and urine kidney injury molecule 1 (KIM-1) were assessed, and renal pathology was analyzed. Apoptotic cells were identified and the apoptotic index was calculated. A rat antibody array was used to analyze expression of cytokines associated with apoptosis. Results from these analyses showed that UHg, RHg, and urine KIM-1, but not SCr, levels were significantly increased in cinnabar-treated rats. Renal pathological changes in cinnabar-treated rats included vacuolization of tubular cells, formation of protein casts, infiltration of inflammatory cells, and increase in the number of apoptotic tubular cells. In comparison to the control group, expression of FasL, Fas, TNF-α, TRAIL, activin A, and adiponectin was upregulated in the cinnabar-treated group. Collectively, our results suggest that prolonged use of cinnabar results in kidney damage due to accumulation of mercury and that the underlying mechanism involves apoptosis of tubular cells via a death receptor-mediated pathway.

scholarly journals Mitigation of cisplatin induced nephrotoxicity by casticin in male albino rats

2023 ◽  
Vol 83 ◽  
Author(s):  
N. Ehsan ◽  
M. U. Ijaz ◽  
A. Ashraf ◽  
S. Sarwar ◽  
A. Samad ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Free Radical Scavenger ◽  
Control Group ◽  
Albino Rats ◽  
Radical Scavenger ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Group 2 ◽  
Kidney Injury Molecule 1

Abstract Cisplatin (CP) is a commonly used, powerful antineoplastic drug, having numerous side effects. Casticin (CAS) is considered as a free radical scavenger and a potent antioxidant. The present research was planned to assess the curative potential of CAS on CP persuaded renal injury in male albino rats. Twenty four male albino rats were distributed into four equal groups. Group-1 was considered as a control group. Animals of Group-2 were injected with 5mg/kg of CP intraperitoneally. Group-3 was co-treated with CAS (50mg/kg) orally and injection of CP (5mg/kg). Group-4 was treated with CAS (50mg/kg) orally throughout the experiment. CP administration substantially reduced the activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione S-transferase (GST), glutathione reductase (GSR), glutathione (GSH) content while increased thiobarbituric acid reactive substances (TBARS), and hydrogen peroxide (H2O2) levels. Urea, urinary creatinine, urobilinogen, urinary proteins, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels were substantially increased. In contrast, albumin and creatinine clearance was significantly reduced in CP treated group. The results demonstrated that CP significantly increased the inflammation indicators including nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activity and histopathological damages. However, the administration of CAS displayed a palliative effect against CP-generated renal toxicity and recovered all parameters by bringing them to a normal level. These results revealed that the CAS is an effective compound having the curative potential to counter the CP-induced renal damage.

scholarly journals Cinnabar Induces Renal Inflammation and Fibrogenesis in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ying Wang ◽  
Dapeng Wang ◽  
Jie Wu ◽  
Bohan Wang ◽  
Liangjun Wang ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Kidney Injury ◽  
Inflammatory Cells ◽  
Control Group ◽  
Mesangial Proliferation ◽  
Renal Inflammation ◽  
Urinary Mercury ◽  
Time Periods ◽  
Kidney Injury Molecule 1 ◽  
Kidney Lesions

The purpose of this study was to investigate whether cinnabar causes renal inflammation and fibrosis in rats. Rats were dosed orally with cinnabar (1 g/kg/day) for 8 weeks or 12 weeks. The control rats were treated with solvent (5% carboxymethylcellulose solution) over the same time periods, respectively. Renal mercury (RHg), urinary mercury (UHg), serum creatinine (SCr), urine kidney injury molecule 1 (KIM-1), renal pathology, and renal mediators were examined. At both 8 weeks and 12 weeks, RHg, UHg, and urine KIM-1 were significantly higher in the cinnabar group than in the control group, although SCr was unchanged. Kidney lesions in the cinnabar-treated rats occurred mainly in the tubules and interstitium, including vacuolization, protein casts, infiltration of inflammatory cells, and slight increase in interstitial collagen. In addition, mild mesangial proliferation was observed in glomeruli. Moreover, the expression of inflammatory and fibrogenic mediators was upregulated in the cinnabar group. In conclusion, cinnabar may cause kidney damage due to the accumulation of mercury, and renal inflammation and slight fibrogenesis may occur in rats. In the clinic, the potential risk of renal injury due to the prolonged consumption of cinnabar should be considered even though the agent is relatively nontoxic.

Coenzyme Q10 Attenuates Cisplatin-induced Nephrotoxicity Through Counteracting Oxidative Stress and Inflammation

2019 ◽  
Vol 6 (1) ◽  
pp. 41-47
Author(s):  
Hala S. Bash ◽  
Ihsan S. Rabeea
Keyword(s):  
Oxidative Stress ◽  
Serum Creatinine ◽  
Coenzyme Q10 ◽  
Kidney Injury ◽  
Treated Group ◽  
Control Group ◽  
Histopathological Analysis ◽  
Adult Rats ◽  
Necrosis Factor Alpha ◽  
Kidney Injury Molecule 1

Background: Cisplatin is an anticancer drug used in the management of solid tumors, however, dose-related nephrotoxicity is one of its major problems. Agents having antioxidants, antiinflammatory and/or antiapoptotic activities may thus represent potential therapeutic options to avoid cisplatin-induced nephrotoxicity. Among these agents, coenzyme Q10 has several pharmacological properties including antioxidant, anti-inflammatory and/or anti-apoptotic effects. Objective: The current study aimed to examine whether coenzyme Q10 could attenuate cisplatininduced nephrotoxicity or not. Methods: 24 adult rats were randomly separated into three groups (8 rats per group). The first one was the control group, rats receiving vehicle (olive oil) intraperitoneally. The second group was Cisplatin treated group, rats were receiving 13 mg/kg of Cisplatin intraperitoneally as a single dose. The third group (Cisplatin + Coenzyme Q10), rats were receiving 13 mg/kg as a single intraperitoneal dose of Cisplatin and coenzyme Q10 daily for six consecutive days (10 mg/kg intraperitoneally). Results: Cisplatin caused significant increases in serum creatinine and severe histological lesions. Cisplatin treated group also showed a significant elevation in renal malondialdehyde concentration as a marker of oxidative stress; renal tumor necrosis factor-alpha concentration as a marker of inflammation; and Kidney injury molecule -1 concentration. Coenzyme Q10 significantly attenuated cisplatininduced nephrotoxicity through lowering serum creatinine and improving nephrotoxicity histological scores. Coenzyme Q10 also significantly reduced the renal concentration of MDA, TNF-α and KIM-1 relative to cisplatin treated group. Conclusions: Coenzyme Q10 has a potential nephroprotective effect against cisplatin-induced nephrotoxicity that was demonstrated by biochemical and histopathological analysis.

scholarly journals Urinary Measurement of Neutrophil Gelatinase Associated Lipocalin and Kidney Injury Molecule-1 Helps Diagnose Acute Pyelonephritis in a Preclinical Model

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Hahn-Ey Lee ◽  
Sun Hee Lee ◽  
Minki Baek ◽  
Hwang Choi ◽  
Kwanjin Park
Keyword(s):  
Acute Pyelonephritis ◽  
Time Course ◽  
Kidney Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Preclinical Model ◽  
Urinary Ngal ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Kidney Injury Molecule 1 ◽  
Neutrophil Gelatinase

Background. The study assessed whether measurement of urinary biomarkers of acute kidney injury could be helpful in diagnosing acute pyelonephritis and subsequent scarring. Method. Escherichia coli J96 (0.3 mL inoculum containing 1×109/mL) was directly injected into the renal cortex of 3-week-old female Sprague Dawley rats (n=20), with saline substituted in a control group (n=10). Following the injection, urine was collected 2, 7, 14, 28, and 42 days after injection. Urinary neutrophil gelatinase associated lipocalin (NGAL), kidney injury molecule-1 (Kim-1), and interleukin-18 were quantitatively measured using enzyme-linked immunosorbent assay (ELISA). The levels of the biomarkers were adjusted for creatinine. Time course changes within a group or between the groups were compared. Correlation analysis was performed to understand the relationship between urinary levels and histological scarring. Results. Significantly elevated urinary NGAL was evident at two and seven days after injection, and Kim-1 was elevated at two days after injection. Receiver operating characteristic analyses confirmed the sensitivity of these markers at these times. No urinary marker at acute stage of APN was correlated with the amount of future scarring, negating their predictive value. Conclusion. Urinary NGAL and Kim-1 could be helpful in diagnosing febrile urinary tract infection in children.

scholarly journals Effect of Pistacia atlantica subsp. kurdica Gum in Experimental Periodontitis Induced in Wistar Rats by Utilization of Osteoclastogenic Bone Markers

Molecules ◽  
2020 ◽  
Vol 25 (24) ◽  
pp. 5819
Author(s):  
Shokhan H. Azeez ◽  
Shanaz M. Gaphor ◽  
Aram M. Sha ◽  
Balkees T. Garib
Keyword(s):  
Wistar Rats ◽  
Bone Markers ◽  
Inflammatory Cells ◽  
Treated Group ◽  
Surrounding Tissue ◽  
Control Group ◽  
Pistacia Atlantica ◽  
Male Wistar Rats ◽  
Experimental Periodontitis ◽  
Serum Rankl

The aim of this study was to assess the effect of local application of essential oil of Pistacia atlantica kurdica (EOK) gel in treatment of experimentally induced periodontitis in rats and its effect on osteoclastogenic bone markers. Twenty-four male Wistar rats of 250 to 350 g were used in this study and were allocated into four groups. Control negative (without induced periodontitis), control positive (induced experimental periodontitis left without treatment), treatment control (induced experimental periodontitis and treated with Chlorhexidine gel) and EOK treated group (induced experimental periodontitis treated with EOK gel). The animals were sacrificed after 30 days, and the mandibular central incisor and surrounding tissue were dissected from the mandible and further processed for preparing H&E slides. Inflammatory cells, osteoclast cells, and periodontal ligament (PDL) were examined and measured histologically. Finally, the mean concentrations of both markers, receptor activator of nuclear factor kappa-Β ligand (RANKL) and (Interleukin-1β) IL-1β, were analyzed by ELISA. A significant reduction of inflammatory reaction and osteoclast numbers with improvement of PDL and low mean concentrations of RANKL and IL-1β were seen in the EOK treated group in comparison to the control group and the chlorhexidine group as well. The extract showed a protective effect in the healing of periodontitis that had been induced in rats and decreased bone resorption by down regulation of serum RANKL and IL-1β markers.

scholarly journals Protein-to-creatinine urinary in the early diagnosis of renal injury in canine pyometra

2019 ◽  
Vol 39 (3) ◽  
pp. 186-191
Author(s):  
Marcos C. Sant’Anna ◽  
Guilherme F. Martins ◽  
Karina K.M.C. Flaiban ◽  
Luiz G.C. Trautwein ◽  
Maria I.M. Martins
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Injury ◽  
Renal Damage ◽  
Systemic Disease ◽  
The Other ◽  
Control Group ◽  
Creatinine Ratio ◽  
Renal Lesions ◽  
Tubular Cells

ABSTRACT: Kidney disease that affects bitches with pyometra may lead patients to develop chronic renal failure even after pyometra treatment. Therefore, several studies have sought to clarify the gaps in the understanding of the pathogenesis of renal injury in pyometra. Identification of early detection markers for renal damage, which can predict and identify the prognosis of the disease, is very important. Proteinuria analysis can diagnose kidney damage, since proteins such as albumin are not filtered through the glomerulus and those that undergo glomerular filtration are almost completely reabsorbed by tubular cells. The objective of this study was to evaluate whether the urinary protein-to-creatinine ratio (UPC) can detect renal injury in bitches with pyometra before development of azotemia. For this, 44 bitches with pyometra were divided into two groups: bitches with azotemic piometra (A, n=15, creatinine >1.7) and bitches with non-azotemic pyometra (NA, n=29). The two groups were compared to the control group (CG, n=12), which had no signs of systemic disease. All animals underwent blood and urine tests. Leukocytosis was more evident in bitches in the A group than in the other groups. This shows that the inflammatory response may be associated with the pathogenesis of renal injury. The median UPC in bitches with pyometra was significantly higher than in the CG, with a median above the reference values. In conclusion, the UPC can be used in bitches with pyometra to detect renal damage before the development of azotemia. It has been suggested that the UPC of bitches with pyometra should be followed through during the postoperative period so that permanent renal lesions secondary to pyometra can be diagnosed and treated properly before the development of azotemia.

scholarly journals Both hyperthermia and dehydration during physical work in the heat contribute to the risk of acute kidney injury

2020 ◽  
Vol 128 (4) ◽  
pp. 715-728 ◽  
Author(s):  
Christopher L. Chapman ◽  
Blair D. Johnson ◽  
Nicole T. Vargas ◽  
David Hostler ◽  
Mark D. Parker ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Core Temperature ◽  
Renal Injury ◽  
Kidney Injury ◽  
Proximal Tubules ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Physical Work ◽  
Control Group ◽  
Water Cooling ◽  
Urine Production

Occupational heat stress increases the risk of acute kidney injury (AKI) and kidney disease. This study tested the hypothesis that attenuating the magnitude of hyperthermia (i.e., increase in core temperature) and/or dehydration during prolonged physical work in the heat attenuates increases in AKI biomarkers. Thirteen healthy adults (3 women, 23 ± 2 yr) exercised for 2 h in a 39.7 ± 0.6°C, 32 ± 3% relative-humidity environmental chamber. In four trials, subjects received water to remain euhydrated ( Water), continuous upper-body cooling ( Cooling), a combination of both ( Water + Cooling), or no intervention ( Control). The magnitude of hyperthermia (increased core temperature of 1.9 ± 0.3°C; P < 0.01) and dehydration (percent loss of body mass of −2.4 ± 0.5%; P < 0.01) were greatest in the Control group. There were greater increases in the urinary biomarkers of AKI in the Control trial: albumin (increase of 13 ± 11 μg/mL; P ≤ 0.05 compared with other trials), neutrophil gelatinase-associated lipocalin (NGAL) (increase of 16 ± 14 ng/dL, P ≤ 0.05 compared with Cooling and Water + Cooling groups), and insulin-like growth factor-binding protein 7 (IGFBP7) (increase of 227 ± 190 ng/mL; P ≤ 0.05 compared with other trials). Increases in IGFBP7 in the Control trial persisted after correcting for urine production/concentration. There were no differences in the AKI biomarker tissue inhibitor of metalloproteinase 2 (TIMP-2) between trials ( P ≥ 0.11). Our findings indicate that the risk of AKI is highest with greater magnitudes of hyperthermia and dehydration during physical work in the heat. Additionally, the differential findings between IGFBP7 (preferentially secreted in proximal tubules) and TIMP-2 (distal tubules) suggest the proximal tubules as the location of potential renal injury. NEW & NOTEWORTHY We demonstrate that the risk for acute kidney injury (AKI) is higher in humans with greater magnitudes of hyperthermia and dehydration during physical work in the heat and that alleviating the hyperthermia and/or limiting dehydration equally reduce the risk of AKI. The biomarker panel employed in this study suggests the proximal tubules as the location of potential renal injury.

scholarly journals Assessment of Urinary Kidney Injury Molecule-1 as an Indicator of Early Renal Insult in Children with Cystic Fibrosis

2020 ◽  
Vol 8 (B) ◽  
pp. 262-267
Author(s):  
Walaa Shahin ◽  
Ahmed Bader ◽  
Rawdah Ahmed ◽  
Mona Alattar ◽  
Mona Alfalaki ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Urine Analysis ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Control Group ◽  
Renal Ultrasound ◽  
Fractional Excretion Of Sodium ◽  
Beta 2 ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

BACKGROUND: The risk of acute kidney injury in cystic fibrosis (CF) patients is due to renal tubular affection by CFTR gene. AIM: Our study aimed at early detection of renal impairment in CF patients, to enable careful monitoring and adjustment of nephrotoxic medications. METHODS: Fifty patients with CF were enrolled in our study; they were age- and sex-matched to 40 healthy control children. All subjects were screened by urine analysis, measurements of kidney function tests, fractional excretion of sodium, β2-microglobulin (beta-2-M) excretion, and renal ultrasound examination. Urinary kidney injury molecule-1 (KIM-1) was assayed using ELISA technique. RESULTS: Both urinary beta-2-M and KIM-1 concentrations were significantly higher in CF patients compared to the control group (p < 0.001). The duration of the disease was significantly positively correlated with the urinary beta-2-M and KIM-1 levels (r = 0.6 and 0.7, respectively; p < 0.01). CONCLUSIONS: Our results showed that urinary KIM-1 can be considered as a sensitive early indicator of acute renal injury.

scholarly journals The effectiveness of Pectin in the reduction of histological changes caused by exposure to monosodium glutamate in female mice: مدى فعالية البكتين في الحد من التغيرات النسيجية التي يسببها تناول جلوتامات أحادي الصوديوم على إناث الفئران

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Sarah Ibrahim Al Othman, Faten khalif Alanazi, Ghada Jaber S
Keyword(s):  
Drinking Water ◽  
Body Weight ◽  
Monosodium Glutamate ◽  
Inflammatory Cells ◽  
Treated Group ◽  
Control Group ◽  
Central Vein ◽  
Histological Changes ◽  
Female Mice ◽  
Liver And Kidney

Monosodium glutamate (MSG) is widely used as a food additive. Excessive consumption of monosodium glutamate has also been shown to affect the liver and kidneys, causing damage to these tissues because of oxidative stress leading to increased production of reactive oxygen species (ROS). The purpose of the study described in this paper was to find out how the liver and kidney toxicity caused by monosodium glutamate can be mitigated using pectin. To this end, 30 albino mice females were divided into four groups. The animals were distributed in special cages. 12-15 weeks with an average body weight of 60 grams. The animals were divided into four groups: the experimental control group (1) comprising 5 female mice were given normal drinking water and the treated group (2) comprising 10 female mice were given monosodium glutamate at a dose of 3 g/kg body weight in drinking water. For three weeks, the treatment group (3) comprising 10 female mice was given pectin at a dose of 300 mg/70 kg body weight in drinking water immediately after the monosodium glutamate dose for three weeks and the pectin group (4) comprising 5 female mice were given Pectin at a dose of 300 mg/70 kg body weight in drinking water for three weeks. The mice were then anesthetized, dissected, and liver and kidney samples were taken from female mice and kept in a 10% neutral formalin solution to make tissue segments. The results showed many histological changes in the liver, such as congestion of the central vein, widening of the sinuses, and the appearance of signs of the death of most hepatocytes, infiltration of the central vein and an invasion of inflammatory cells around the central vein with the emergence of several gaps within the cells. Many of them cavity with the death of most of the tubule cells, the closure of some of them and the expansion and infiltration in others and bleeding inside the tissue. Pectin therapy has led to the disappearance of most of these changes and the emergence of a clear improvement in hepatic and renal tissue.

scholarly journals Enhancing acute kidney injury regeneration by promoting cellular dedifferentiation in zebrafish

2018 ◽  
Author(s):  
Lauren Brilli Skvarca ◽  
Hwa In Han ◽  
Eugenel B. Espiritu ◽  
Maria A. Missinato ◽  
Elizabeth R. Rochon ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Injury ◽  
Cardiac Injury ◽  
Kidney Injury ◽  
Acute Injury ◽  
Cardiomyocyte Proliferation ◽  
Deacetylase Inhibitor ◽  
Summary Statement ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

ABSTRACTAcute kidney injury (AKI) is a serious disorder for which there is no approved pharmaceutical treatment. Following injury, native nephrons display limited regenerative capabilities, relying on the dedifferentiation and proliferation of renal tubular epithelial cells (RTECs) that survive the insult. Previously, we identified 4-(phenylthio)butanoic acid (PTBA), a histone deacetylase inhibitor (HDI) that enhances renal recovery and showed that PTBA treatment increased RTEC proliferation and reduced renal fibrosis. Here, we investigated the regenerative mechanisms of PTBA in zebrafish models of larval renal injury and adult cardiac injury. With respect to renal injury, we showed that delivery of PTBA using an esterified prodrug (UPHD25) increases the reactivation of the renal progenitor gene Pax2a, enhances dedifferentiation of RTECs, reduces Kidney injury molecule-1 expression, and lowers the number of infiltrating macrophages. Further, we find that the effects of PTBA on RTEC proliferation depend upon retinoic acid signaling and demonstrate the therapeutic properties of PTBA are not restricted to the kidney but also increase cardiomyocyte proliferation and decrease fibrosis following cardiac injury in adult zebrafish. These studies provide key mechanistic insights into how PTBA enhances tissue repair in models of acute injury and lay the groundwork for translating this novel HDI into the clinic.SUMMARY STATEMENTMortality associated with acute kidney injury (AKI) is in part due to limited treatments available to ameliorate kidney injury. We identified a compound that enhances AKI recovery by promoting cellular dedifferentiation.

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