Necrosis Of Renal Tubules Research Articles

Methanolic Extract of Cannabis sativa Ameliorates Rifampin-Induced Nephrotoxicity and Tubular Necrosis in Rats

Purpose: The study was conducted for the renal protective activity of the methanolic extract of Cannabis sativa against renal toxicity induced by rifampin injection in rats. This study selected Cannabis sativa, a member of the Cannabinaceae family, for its widespread use in treating gout, constipation, pain, insomnia, kidney inflammation, and other diseases. The results showed decreased levels of serum urea, creatinine, sodium (Na), and potassium (K) inhibited the induced toxicity. Histopathological examination revealed that the kidney was protected from the marked necrosis of renal tubules caused by rifampin. Methodology: Forty Wister white (albino) rats weighing 100-150 gm were used. We produced renal toxicity by injecting rifampin i/p- at a dose rate of 0.8 mL/kg BW for 28 days, which led to nephrotoxicity. We administered the plant extract by simultaneously administering a methanolic extract of Cannabis sativa orally at dose rates of 300 and 600 mg/kg for 28 days. Findings: Rifampin-induced nephrotoxicity increased potassium, urea, and creatinine levels while decreasing sodium levels. When Cannabis sativa is administered with rifampin, sodium concentrations increase. A decrease in potassium, urea, and creatinine accompanies the increase in sodium levels. Unique Contribution to Theory, Practice, and Policy: Flavonoids may be responsible for the nephroprotective effect of Cannabis sativa extract; therefore, more research to identify the active component is necessary.

Hypogalactia as a cause of neonatal hypernatremia

Neonatal hypernatremia is a condition in which the concentration of sodium in the blood of a newborn child exceeds 145 mmol/l. The causes of this pathology may be kidney disease, endocrine problems, transdermal water loss, iatrogenic sodium overload. In addition, dehydration due to insufficient breastfeeding remains one of the important factors leading to hypernatremia. Clinical signs include: significant weight loss, decreased skin turgor, anxiety, fever, seizures, and direct hyperbilirubinemia. The main complications of this condition are intracranial hemorrhages, venous sinus thrombosis and acute renal tubule necrosis. Infusion therapy and adequate oral nutrition are used to correct hypernatremia. The article presents a clinical case of hypernatremia in a newborn child caused by hypogalactyly in the mother. The purpose of the demonstration is to raise awareness and alertness among pediatricians and neonatologists about the possibility of this problem.

The Salutary Effects of Diminazene, Lisinopril or Valsartan on Cisplatin – Induced Acute Kidney Injury in Rats: A Comparative Study

Nephrotoxicity as a cause of acute kidney injury (AKI) induced by cisplatin (CP), limits its usefulness as an anticancer agent. Diminazene, an angiotensin converting enzyme 2 activator, exhibited renoprotective properties on rat models of kidney diseases. This research aims to investigate the salutary effect of diminazene in comparison with lisinopril or valsartan in CP-induced AKI. The first and second groups of rats received oral vehicle (distilled water) for 9 days, and saline injection or intraperitoneal CP (6 mg/kg) on day 6, respectively. Third, fourth, and fifth groups received intraperitoneal injections of CP on day 6 and diminazene (15 mg/kg/day, orally), lisinopril (10 mg/kg/day, orally), or valsartan (30 mg/kg/day, orally), for 9 days, respectively. 24h after the last day of treatment, blood and kidneys were removed under anesthesia for biochemical and histopathological examination. Urine during the last 24 h before sacrificing the rats was also collected. CP significantly increased plasma urea, creatinine, neutrophil gelatinase-associated lipocalin, calcium, phosphorus, and uric acid. It also increased urinary albumin/creatinine ratio, N-Acetyl-β-D-Glucosaminidase/creatinine ratio, and reduced creatinine clearance, as well the plasma concentrations of inflammatory cytokines [plasma tumor necrosis factor–alpha, and interleukin-1beta], and significantly reduced antioxidant indices [catalase, glutathione reductase , and superoxide dismutase]. Histopathologically, CP treatment caused necrosis of renal tubules, tubular casts, shrunken glomeruli, and increased renal fibrosis. Diminazine, lisinopril, and valsartan ameliorated CP-induced biochemical and histopathological changes to a similar extent. The salutary effect of the three drugs used is, at least partially, due to their anti-inflammatory and antioxidant effects. Keywords: Cisplatin • Diminazene • ACE2 activator • Lisinopril • Valsartan • Acute kidney injury

Nephroprotective effects of diminazene on doxorubicin-induced acute kidney injury in rats

This study aimed to investigate the potential protective effects of diminazene, an activator of angiotensin II converting enzyme (ACE2), on kidney function and structure in rats with acute kidney injury (AKI) induced by the anticancer drug doxorubicin (DOX). The impact of diminazene was compared to that of two other drugs: the ACE inhibitor lisinopril and the angiotensin II type 1 (AT1) receptor blocker valsartan. Rats were subjected to a single intraperitoneal injection of DOX (13.5 mg/kg) on the 5th day, either alone or in combination with diminazene (15 mg/kg/day), lisinopril (10 mg/kg/day), or valsartan (30 mg/kg/day) for 8 consecutive days. Various markers related to kidney function, oxidative stress, and inflammation were measured in plasma and urine. Additionally, kidney tissues were assessed histopathologically. DOX-induced nephrotoxicity was confirmed by elevated levels of plasma urea, creatinine, and neutrophil gelatinase-associated lipocalin (NGAL). DOX also led to increased urinary N-acetyl-β-D-glucosaminidase (NAG) activity and decreased creatinine clearance, albumin levels, and osmolality. Moreover, DOX caused a reduction in renal oxidative stress markers, including superoxide dismutase (SOD), glutathione reductase (GR), and catalase activities, while increasing malondialdehyde (MDA) levels. It also raised plasma inflammatory markers, tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β). Concurrently administering diminazene significantly mitigated these DOX-induced changes, including histopathological alterations like renal tubule necrosis, tubular casts, shrunken glomeruli, and increased renal fibrosis. Similar protective effects were observed with lisinopril and valsartan. These protective effects, at least in part, appear to result from the anti-inflammatory and antioxidant properties of these drugs. In summary, this study suggests that the administration of diminazene, lisinopril, or valsartan had comparable effects in ameliorating the biochemical and histopathological aspects of DOX-induced acute kidney injury in rats.

English

Pesticides especially insecticides are widely used in the field of agricultural development all over the world to increase crop production. Moreover, exposure to such compounds does not only influence the intended targets but also induces adverse impacts on a number of unintended targets in animals. This research aimed to determine the toxic impacts of lufenuron (an insecticide) on the health status of fish in terms of measurement of oxidative stress, antioxidant enzymes, DNA damage and histopathological changes in Nile tilapia (Oreochromis niloticus) exposed to different concentrations. For this purpose, Oreochromis niloticus fish, weighing about 75-80g were arbitrarily separated into four different groups and then exposed to lufenuron @ 0.7, 1.2 and 1.7µg/ L for 39 days. The results showed that the fish exposed to the pesticide had significant changes in oxidative stress, antioxidant profile in gills and percentile rate of DNA damage in different visceral organs including liver, kidney, and gills. Results of light microscopic investigations indicated different histological changes in liver (necrosis of hepatocytes, degeneration of hepatocytes, vacuolar degeneration and congestion), gills (necrosis of lamellar epithelial cells, telangiectasia, and atrophy of secondary lamellae), heart (congestion, necrosis of neurons, microgliosis and intracellular edema), brain (congestion, myofibrosis, neutrophilic and myocarditis) and kidneys (necrosis of renal tubules, widening of urinary space, necrosis of renal tubular epithelial cells). A significantly escalate in oxidative stress while lower quantity of antioxidant biomarkers was documented in experimental fish. The findings of this study suggest that long-term exposure to lufenuron has negative health effects via induction of DNA damage, increased oxidative stress, lowering of enzymatic antioxidants profile and histological lesions in visceral organs of Nile tilapita (Oreochromis niloticus).

The effect of diminazene, an angiotensin-converting enzyme 2 activator, on adenine-induced chronic kidney disease in rats.

The present study investigated the effect of diminazene, lisinopril, or valsartan on adenine-induced chronic kidney disease (CKD) in rats. The animals were divided into five groups (n= 6). The first and second groups received normal diet and adenine in the feed at a dose of 0.25% w/w for 35 days, respectively. The third, fourth, and fifth groups were treated as the second group but also received diminazene (15 mg/kg/day), lisinopril (10mg/kg/day), and valsartan (30 mg/kg/day), respectively, for 35 days. Adenine significantly increased plasma urea, creatinine, neutrophil gelatinase-associated lipocalin (NGAL), calcium, phosphorus, and uric acid. In addition, adenine increased urinary albumin/creatinine ratio and N-Acetyl-β-D-glucosaminidase (NAG)/creatinine ratio and reduced creatinine clearance. Adenine also significantly increased the plasma concentrations of inflammatory cytokines (plasma tumor necrosis factor-alpha [TNF-α] and interleukin-1beta [IL-1β]) and significantly reduced antioxidant indices (catalase, glutathione reductase [GR], and superoxide dismutase [SOD]). Histopathologically, renal tissue from adenine-treated rats showed necrosis of renal tubules, tubular casts, shrunken glomeruli, and increased renal fibrosis. All drugs ameliorated adenine-induced biochemical and histopathological changes. The protective effect of the three drugs used is, at least partially, due to their anti-inflammatory and antioxidant effects. Our results show that administration of diminazene, lisinopril, or valsartan had a comparable effect on the reversal of the biochemical and histopathological indices of adenine-induced CKD in rats.

Clinicohematological, Mutagenic, and Oxidative Stress Induced by Pendimethalin in Freshwater Fish Bighead Carp (Hypophthalmichthys nobilis).

Currently, aquatic and terrestrial ecosystems are continuously and chronically polluted by cocktails of countless chemical compounds. The susceptibility to infections is tremendously increasing in a variety of organisms due to exposure to environmental pollutants. Pendimethalin, an herbicide, is continuously used in agriculture to remove unwanted broadleaf weeds across the globe. Therefore, this study investigates the mechanisms of toxicity of pendimethalin in freshwater fish bighead carp upon exposure to low and environmentally relevant concentrations. For this purpose, 48 fish without any clinical abnormalities were kept in a glass aquarium in different experimental groups (T0, T1, T2, and T3). These groups were treated with pendimethalin at 0.00, 0.25, 0.50, and 0.75 mg/L, respectively. Four fish were randomly picked from each experimental group and killed at 72, 96, and 120 hours of the trial to study hematobiochemical parameters and visceral tissues including the brain, liver, heart, gills, and kidneys for histopathology. Herbicide-treated fish indicated various physical and behavioral abnormalities including hypersecretion of mucus, erratic swimming, operculum movement, air gulping, tremors of fins, loss of equilibrium, and increased surface breathing. Histopathologically, gills tissues of treated fish indicated atrophied lamellae, uplifting of secondary lamellae, necrosis of primary and secondary lamellar epithelial cells, telogenesis, congestion, and lamellar fusion. Histopathological examination of liver tissues of treated fish showed mild to moderate congestion, necrosis of hepatocytes, and atrophy of hepatocytes while kidneys revealed degeneration of renal tubules, glomerular atrophy, ceroid, and necrosis of renal tubules. The erythrocyte counts, monocyte and lymphocyte counts, and hemoglobin values were significantly (P < 0.05) reduced in pendimethalin-treated fish. Results on serum biochemistry showed that the biomarkers of kidneys, heart, and liver were significantly higher in fish of treated groups. In addition, values of different biochemical reactions like reactive oxygen species (ROS), thiobarbituric acid reactive species (TBARS), total proteins, and quantity of different antioxidant enzymes including reduced glutathione (GSH), catalase, and superoxide dismutase (SOD) were significantly different when compared to untreated fish. Moreover, the percentile of different nuclear abnormalities in red blood cells and frequency of DNA damage increased significantly in treated fish. It can be concluded from the findings that pendimethalin causes its toxic effects via disruption of physiological and hematobiochemical reactions of fish.

Hematobiochemical, Oxidative Stress, and Histopathological Mediated Toxicity Induced by Nickel Ferrite (NiFe2O4) Nanoparticles in Rabbits.

From the past few decades, attention towards the biological evaluation of nanoparticles (NPs) has increased due to the persistent and extensive application of NPs in various fields, including biomedical science, modern industry, magnetic resonance imaging, and the construction of sensors. Therefore, in the current study, magnetic nickel ferrite (NiFe2O4) nanoparticles (NFNPs) were synthesized and evaluated for their possible adverse effects in rabbits. The crystallinity of the synthesized NFNPs was confirmed using X-ray diffraction (XRD) technique. The saturation magnetization (46.7 emug−1) was measured using vibrating sample magnetometer (VSM) and 0.35-tesla magnetron by magnetic resonance imaging (MRI). The adverse effects of NFNPs on blood biochemistry and histoarchitecture of the liver, kidneys, spleen, brain, and heart of the rabbits were determined. A total of sixteen adult rabbits, healthy and free from any apparent infection, were blindly placed in two groups. The rabbits in group A served as control, while the rabbits in group B received a single dose (via ear vein) of NFNPs for ten days. The blood and visceral tissues were collected from each rabbit at days 5 and 10 of posttreatment. The results on blood and serum biochemistry profile indicated significant variation in hematological and serum biomarkers in NFNP-treated rabbits. The results showed an increased quantity of oxidative stress and depletion of antioxidant enzymes in treated rabbits. Various serum biochemical tests exhibited significantly higher concentrations of different liver function tests, kidney function tests, and cardiac biomarkers. Histopathologically, the liver showed congestion, edema, atrophy, and degeneration of hepatocytes. The kidneys exhibited hemorrhages, atrophy of renal tubule, degeneration, and necrosis of renal tubules, whereas coagulative necrosis, neutrophilic infiltration, and severe myocarditis were seen in different sections of the heart. The brain of the treated rabbits revealed necrosis of neurons, neuron atrophy, and microgliosis. In conclusion, the current study results indicated that the highest concentration of NPs induced adverse effects on multiple tissues of the rabbits.

Histopathological Changes in Some Vital Organs of Nursery Pigs in Mortalities Associated with African Swine Fever Outbreak

African swine fever (ASF) is a contagious viral disease that affects domestic and wild pigs. The disease is of serious economic importance as outbreaks lead to the culling of millions of pigs in Africa, Eastern Europe and some parts of Asia. The present study evaluated the histopathological changes in some visceral organs in nursery pigs infected with ASF virus. The pigs were euthanized in carbon dioxide chamber and necropsied. Tissue samples were fixed in 10% neutral buffered formalin, routinely processed, sectioned at 5µm thickness and stained with hematoxylin and eosin (H&amp;E). Results showed petechial and ecchymotic hemorrhages grossly on the skin and in the lungs, heart, spleen, lymph nodes, and kidneys. In the heart, there was hydropericardium and the pericardial sac was cloudy. The liver was also enlarged and mottled. Microscopically, hemorrhages were present in the lungs, heart, lymph nodes, and kidneys. There was interstitial pneumonia and necrosis of renal tubules. Severe lymphoid necrosis occurred in the spleen. It was concluded that the disease involved a moderately pathogenic isolate of ASF virus and that hemorrhages in visceral organs and destruction of lymphoid tissues remained the major findings in sub-acute ASF infection.

Virulence factor genes and comparative pathogenicity study of tdh, trh and tlh positive Vibrio parahaemolyticus strains isolated from Whiteleg shrimp, Litopenaeus vannamei (Boone, 1931) in India.

Vibrio parahaemolyticus is a gram-negative halophilic bacterium responsible for gastrointestinal infection in human and vibriosis in aquatic animals. The thermostable direct hemolysin (tdh), tdh-related hemolysin (trh) and thermolabile hemolysin (tlh) positive strains of V. parahaemolyticus were identified from brackishwater aquaculture farms of West Bengal and Andhra Pradesh, India. Moreover, the presence of other virulent genes like vcrD1, vopD, vp1680 under type three secretion system 1 (T3SS1) and vcrD2 vopD2, vopB2, vopC2 under type three secretion system 2 (T3SS2) were detected in tdh positive strain of V. parahaemolyticus. Furthermore, the study revealed that the tdh and trh positive isolates were resistant to β-lactam antibiotics and were able to lyse more than 95% of human Red Blood Cells (RBCs). In addition, both the isolates showed high cytotoxicity in Human Embryonic Kidney (HEK) cell line compared to tlh positive strain. Additionally, intraperitoneal and oral administration of tdh and trh positive strain of V. parahaemolyticus in Indian Major Carp, Labeo rohita caused 100% mortality at the level of 2.0×108CFUml-1 and 1.6×108CFUml-1, respectively. In contrast, only 10% mortality was observed in the case of tlh positive strain at the level of 2.5× 108CFUml-1. The histopathological changes like infiltration of blood cells and degenerated hepatic tissue in the liver of L. rohita were observed after the experimental challenge. The changes like degeneration of glomeruli, necrosis of renal tubules and Bowman's capsule were observed in the kidney section. Ragged, irregular shaped villi and necrosis of the villus were observed in the intestinal lumen. Overall, the study demonstrates that isolated V. parahaemolyticus is a potent aquatic microbial pathogen. Additionally, as V. parahaemolyticus is also a human pathogen and might pose a threat to the human population, proper management strategies are required to prevent the possible occurrence of disease.

Histopathological Study of Liver and Kidney Tissues in C57 Mice via Chronic Exposure to Cadmium and Zinc.

Heavy metals have a wide application in the industrial world, affecting the health and longevity of living organisms. The current study assessed the possible effects of Cadmium (Cd) and Zinc (Zn) on the liver and kidney. Therefore, 150 male and female white mice C57BL were treated in three different groups with 0.685 mg/L CdCl2. 2.5H2O (group 1), and 0.567 mg/L ZnSO4.7H2O (group 2) in drinking water, while the control group only received water for 90 days to investigate how these elements accumulated in the liver/kidney and evaluate the possible histological changes in the liver and kidney. During 90 days, the histopathological consequences of Cd and Zn on the liver and kidneys were recorded. The results pointed out that exposure to heavy metals, such as Cd and Zn, led to organ accumulation of these elements. The histological evaluations demonstrated significant detrimental effects on the liver and kidney. Under the influence of Cd, light microscopic examination revealed significant histological alterations in both organs. In the animals exposed to Cd and Zn, histopathological alterations were observed in the liver, including extensive degeneration, necrosis, depletion, and necrosis of hepatocytes with significant nuclear hypertrophy. When animals are exposed to Cd and Zn, histological alterations in the kidneys include severe vascular degeneration and renal tubule necrosis. In conclusion, heavy metal intoxication has been shown to cause histopathological changes in the liver and kidneys of experimental animal models.

Effect addition of Cinnamomum cassia on treatment of pathological infections in Cyprinus carpio L. fingerlings

The goal of this study was to isolate and identify the causative agents that causes death in Yankee Hatch / Erbil fingerling Cyprinus carpio and to investigate the effect of Cinnamon on the infected fish handled. Both Staphylococcus aureus and Escherichia coli are strongly isolate followed by Aeromonas hydrophila and Klebsiella pneumonia were isolated from liver, kidney and intestine which cause histopathological changes in these organs, characterized by fibrosis in liver, coagulative necrosis in renal tubules in the kidney and sever enteritis. Cinnamomum cassia added to the ration of infected fish at concentration 0.75, 1 and 1.5 %for eight weeks. The histopathological examination reveals that the 1.5% is best the percentage used as food additive for repair and regenerative tissue damage in the liver, kidney and intestine. These study conclude that C. cassia have been used as additive food in fish feed ration at 1.5% and have important role in regenerative tissue damage and keep fish in health status.

The Potential Teratogenic Effect of Tilmicosin in Rats: Visceral Malformations and Histomorphological Alterations in Fetal Internal Organs

Potential fetal adverse effects are well-known for several antibacterial classes. The present study was performed to evaluate the potential teratogenic effect of Tilmicosin (TMS) antibiotic in Sprague Dawley rats. TMS was daily administered orally to pregnant rats at two dose levels, 250 or 500 mg/kg bw, on 6-15 days of gestation. The morphological or skeletal malformations were non-significantly different from control values. However, visceral examination revealed elevation in the percentage of intrathoracic and intracranial haemorrhages, and kidney hypoplasia (unilateral or bilateral) in fetuses from dams treated with the high dose. In addition, both dose levels produced fetuses with increased percentages of dilated brain ventricles, heart ventricles and renal pelvis. Histopathologically, both TMS doses induced pathological changes in fetal liver and kidney, in a dose-dependent manner. Liver showed hepatocyte hydropic degeneration, congestion of hepatic blood vessels, engorgement of bile canaliculi and dilatation of hepatic lymphatic vessels. Kidney revealed coagulative necrosis of renal tubules and glomerular tuft, adhesion between the parietal and visceral layers of Bowman’s capsule and the glomerular tuft became ring shape with the presence of multiple layer glomerular tufts. In conclusion, TMS antibiotic has the potential to induce teratogenic effects (mainly visceral) and pathological changes in liver and kidneys tissues of rat fetuses when administered during the organogenesis period. This result demonstrated the ability of TMS to pass the placental barrier.

Localization of goose haemorrhagic polyomavirus in naturally infected geese using in situ hybridization

ABSTRACT Goose haemorrhagic polyomavirus (GHPV) is the aetiological agent of haemorrhagic nephritis enteritis of geese (HNEG), a fatal disease that impacts geese and has been recorded only in Europe. The present study describes the first clinical cases of HNEG in Taiwan and the phylogenesis of Taiwanese GHPV, and it elucidates the pathogenesis of GHPV infection using in situ hybridization (ISH). The genomes of Taiwanese GHPV were highly similar to the previously reported strains. The diseased geese showed various degrees of vascular damage, especially in the digestive tract. The affected geese in the early stage showed transmural haemorrhagic enteritis in the intestine. In the middle to late stages, the most obvious lesion was hypoxic necrosis of renal tubules around intralobular central veins. Mineralization deposited in the kidney and systemic gout were also found. ISH revealed GHPV DNA in the vascular endothelial cells throughout the body, but not in the parenchymal cells of organs. Accordingly, the pathogenesis of GHPV infection was consistent with viral tropism in the endothelial cells. Specific attack of vascular endothelium by GHPV resulted in endothelial cell necrosis and subsequent increases of blood vessel permeability, as well as secondary circulation disorders, such as oedema, haemorrhage, and ischaemic necrosis in the adjacent parenchyma. RESEARCH HIGHLIGHTS Cell tropism of GHPV is determined by in situ hybridization. The tropism results in vascular dysfunction and subsequent pathobiology. Haemorrhagic nephritis and enteritis of geese described outside Europe for the first time.

Comparing alpha-cypermethrin induced dose/gender-dependent responses of lizards in hepatotoxicity and nephrotoxicity in a food chain

Pesticides are proposed as one reason for the worldwide decline in the reptile. Effects of pesticides on food intake and organ toxicity could affect wildlife populations dynamics. To explore the hepatotoxicity of alpha-cypermethrin (ACP) in reptiles, we designed a tri-trophic food chain with three concentrations (0, 2, and 20 mg/kgwet weight). Although the enzymes changes were similar between male and female lizards, the significant variations in anti-oxidative enzymes’ activities, lactic dehydrogenase activities and acetylcholine esterase activities in liver and kidney suggesting that oxidative stress, decreased metabolic ability and neurotoxicity on lizards. The results of hepatic metabolomics showed that ACP could affect amino acid, energy and lipid metabolism on lizards. Comparing with female lizards, there were more significant changes of metabolites in male lizards. The histopathology analysis in the liver (such as hepatic lobule congestion and hepatocyte vacuolation) and kidney (such as renal tubule necrosis and glomerulus necrosis), dose- and gender dependent changes of lesions suggested the functions of organ were damaged. In summary, the reduction of detoxification and elimination capacities of the liver and kidney showed dose/gender-dependent in lizards.

Key genes of renal tubular necrosis: a bioinformatics analysis

BackgroundTo explore the key genes in renal tubular necrosis.MethodsMicroarray datasets GSE69644, GSE27168, and GSE2027 were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified and we performed functional enrichment analysis. The network of protein interaction and gene interaction was constructed, and the module analysis was conducted using Cytoscape.ResultsA total of 543 DEGs and 13 hub genes were identified. The correlation analysis between the hub genes and the clinical characteristics of tubular necrosis indicated that the patients with high expression of SPAG5 and BIRC5 had better renal function. Patients with high expression of KIF14, KIF20A, MAD2L1, CKAP2, CDC25C, and CENPEN had poor renal function. Four of those hub genes participate in the cell cycle, apoptosis, and mismatch repair by regulating important genes in the pathway.ConclusionsOur study suggests that CDC25C, MAD2L, BIRC5, and EXO1 participate in the cell cycle, apoptosis, and mismatch repair during renal tubule necrosis (RTN) and have an impact on renal function.

Effect of electroacupuncture on renal fibrosis in spontaneously hypertension rats and its related mechanisms

To observe the effect of electroacupuncture (EA) on blood pressure, renal fibrosis and expression of tissue inhibitors of metalloproteinase-1 (TIMP-1), plasminogen activator inhibitor 1 (PAI-1), and alpha smooth muscle actin (α-SMA) in spontaneous hypertension rats (SHR), so as to explore its mechanisms underlying improving hypertensive renal damage. Forty male SHR (15 weeks in age) were randomly divided into 5 groups: model, medication (Losartan), Shenshu, Geshu, and Shenshu＋Geshu groups(n=8 rats in each group), and the same age-old male 8 Wistar-Kyoto (WKY) rats were used as the normal control group. Rats of the medication group were treated by gavage of Losartan potassium solution (3 mg/mL, 30 mg·kg-1·d-1, once a day for 12 weeks), and those of the 3 EA groups treated by EA stimulation of bilateral "Shenshu" (BL23), "Geshu"(BL17) or both BL23 and BL17 (2 Hz/100 Hz, 1 mA, 15 min each time, once every other day for 12 weeks). The systolic blood pressure of the tail artery was measured before, and 4, 8 and 12 weeks after the intervention. The expression of TIMP-1, PAI-1 and α-SMA proteins of the right kidney tissue was measured by immunohistochemistry. Histopathological changes of the right renal tissue were observed under light microscope after H.E. stain. The blood pressure was significantly higher in the mo-del group than those in the normal control group (P<0.01), and considerably decreased at the 4th , 8th, and 12th week of the interventions in the medication and 3 EA groups (P<0.01). The expression levels of renal TIMP-1, PAI-1 and α-SMA proteins were notably higher in the model group than those in the normal control group and considerably decreased at the 12th week of the interventions in the medication and 3 EA groups than in the model group (P<0.01). H.E. staining of the renal tissue showed disordered arrangement of the renal cells, congestion and dilation of capillaries with thickened vascular wall, renal tubule atrophy and lumen stenosis with some necrosis of renal tubules, protein tubule and cell tubules, increase of some glomerular mesangial matrix and hyperplasia of fibrous tissue in the model group, which was re-latively milder in the medication and 3 EA groups. EA of BL23 and BL17 can reduce the blood pressure in SHR, which may be related to its function in down-regulating expression of TIMP-1, PAI-1 and α-SMA proteins.

The Role of Black Soybean and Purple Sweet Potato Active Compound on Advanced Glycation End-Product in Streptozotocin-Induced Type 2 Diabetes Mellitus Rat

Diabetic nephropathy is one of the diabetes complications attacking kidney leading to kidney damage. Hyperglycemia accompanying DM causes the increase of Ad-vanced Glycation End-Product (AGE) and Receptor Advanced Glycation End-Product (RAGE) activity, then develop kidney damage and other diabetes compli-cations. The study aimed to investigate the effect of black soybean, purple sweet potato, or their combination on the expression of AGE, RAGE, and kidney necro-sis T2DM model rats. The rats were given with high-calorie diet for five weeks and then injected with a low dose of streptozotocin (30 m/kg Body Weight) in intraperitoneal. DM rats were divided into: normal, K- (T2DM), K+ (T2DM + glibenclamide 0.6 mg/kg body weight), P1 (T2DM + black soybean), P2 (T2DM + purple sweet potato), and P3-5 Combination 1-3 (T2DM + combination of black soybean and purple sweet potato in ratio of 1 : 3, 2 : 2, and 3 : 1). DM rats were then given the treatments for thirty days. The effect of black soybean, purple sweet potato, or the combination of both was evaluated through the expression of AGE, RAGE, and necrosis of renal tubules. The changes in renal tubules histological characteristics were evaluated using hematoxylin-eosin (HE) staining. Immuno-histochemistry analysis of renal tubules was to evaluate AGE-RAGE expression after the treatments. The research results indicated that there was a significant dif-ference from the combination of black soybean and purple sweet potato in reduc-ing AGE, RAGE, and renal tubules necrosis. The BSB and PSP combination ratio of 1:1 was able to improve renal tubules, decrease the expression of AGE and RAGE towards near normal. The combination of black soybean and purple sweet potato could be used as one of the alternatives to improve kidney damage in dia-betic nephropathy.

CHRONIC INTERACTION BETWEEN METFORMIN AND MELOXICAM IN MICE

Objective: This study is performed for investigation the chronic interaction between metformin and meloxicam from toxicological view.&#x0D; Methods: Lethal dose 50 after chronic exposure assessed in mice by up and down method. Their interaction analyzed by isobolographic analysis indicated that both medicines exhibited synergism. Assessment of the effects of repeated chronic dosing for 3 months of both medicines also performed on mice. Medicines in question administered orally as therapeutic doses of metformin 14 mg/kg. Body weight (BW) (G1), meloxicam 0.2 mg/kg.BW (G2), and combination of both medicines (G3) while G4 assigned control and dosed DW.&#x0D; Results: Both G1 and G3 showed significant p˂0.05 decrease in blood glucose and serum cholesterol levels. Meloxicam group (G3) showed statistically significant p˂0.05 increase in triglycerides and alanine aminotransferase (ALT), and aspartate aminotransferase (AST), while group of combination showed statistically significant p≤0.05 decrease in both ALT and AST. Blood urea nitrogen, uric acid, and serum creatinine showed statistically significant p˂0.05 increase in group of meloxicam but decrease in G3 and no changes in G1. Histopathological changes included variable lesions in kidney such as swelling and necrosis in renal tubules of metformin group, cortical vacuolar degeneration in renal tubules, and deterioration of most glomeruli in G2, while G3 showed generalized cortical necrosis of renal tubules and interstitial nephritis. Liver lesions included central venous congestion (VC) and perivascular lymphocytic infiltration and marked necrosis in both groups of metformin and meloxicam, while there were severe VC and necrosis of hepatocytes in group of combination.&#x0D; Conclusion: Metformin administration with meloxicam may have beneficial important through preventing many deleterious effects of meloxicam after long-standing administration, but adjusting dosing regimen study might be recommended.

Nephrotoxic Effect of Antipsychotic Drug Risperidone: Protective Role Extract of Urtica dioica leaf in Male Stressed Rats

This research was designed to investigate the ameliorative effect of Urtica dioica leaf extract on the kidney function against Risperidone. Thirty adult male rats were randomly divided to 3 equal group and handles as follows for 4th weeks: control group were administered tap water group G1; group G2 rats of this group had been administered risperidone 2 mg/kg orally only; group G3 rats of this group had been administered risperidone 2 mg/kg orally plus ethanolic extract of Urtica dioica (100 mg/kg). Blood sample were obtained at 15 and 30 days of the experiments for estimation of serum uric acid concentration, serum urea nitrogen concentration, serum creatinine concentration, serum peroxynitrite concentration. Significant increases in estimated parameters in group G2 (risperidone treated group). On the other hand, the results showed the beneficial effects of Urtica dioica leaf extract to improvement the previous parameters against risperidone (G3), through a significant decrease in concentrations. Histological section show atrophy and acute necrosis in renal tubules in group G2, while no clear pathological lesion in G3 group. Therefore, it could be conclude that Urtica dioica exert a protective action to alleviating the oxidative stress induced by risperidone stressed rats.