scholarly journals Ameliorative Effects of Gallic Acid on Cisplatin-Induced Nephrotoxicity in Rat Variations of Biochemistry, Histopathology, and Gene Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zahra Eslamifar ◽  
Abbas Moridnia ◽  
Susan Sabbagh ◽  
Reza Ghaffaripour ◽  
Leila Jafaripour ◽  
...  
Keyword(s):  
Gene Expression ◽  
Uric Acid ◽  
Single Dose ◽  
Gallic Acid ◽  
Biochemical Parameters ◽  
Standard Condition ◽  
Renal Tissue ◽  
Control Group ◽  
Male Wistar Rats ◽  
Histopathological Studies

Background. Cisplatin is a powerful chemotherapeutic drug mainly used in the treatment of solid tumors. Aggregation of the drug in renal proximal tubule cells causes nephrotoxicity and renal failure. Investigations showed nephrotoxicity as Cisplatin’s dose-limiting side effect. One of the Cisplatin toxicity mechanisms is generation of reactive oxygen species, which leads to oxidative stress and renal damage. The purpose of this study was evaluation of the modulating effects of Gallic acid on Cisplatin-induced variations including Caspase-3 and Clusterin expression and histopathological and biochemical parameters in adult male Wistar rats. Method. Rats were kept under standard condition of temperature, light, and humidity. The animals were divided into 4 groups: GpI: control group (received distilled water for 10 days); GpII: Gallic acid (alone) (50 mg/kg bw, once a day for 10 days); GpIII: Cisplatin (alone), single dose (6 mg/kg bw, I.P. on 5th day of study); GpIV: Gallic acid (50 mg/kg bw, once a day for 10 days) and also injected with single dose of Cisplatin (6 mg/kg bw, I.P., on 5th day of study). After 10 days, all rats were anaesthetized and plasma collected to estimate urea, creatinine, and uric acid. The right kidneys were removed for the study of gene expression and biochemical parameters. The left kidneys were used for histopathological studies. Results. The Cisplatin-induced nephrotoxicity was evident from the elevated levels of creatinine, urea, uric acid, and renal tissue MDA and also decreased levels of SOD, CAT, GPX, and GSH in renal tissue. Administration of Gallic acid significantly modulated nephrotoxicity markers, gene expression variations, and histopathological damage. Conclusion. Outcomes of the present investigation suggest that Gallic acid provides protection against CP-induced nephrotoxicity, but for application in people, further studies are needed.

Short-term effects of troxerutin (vitamin P4) on muscle fatigue and gene expression of Bcl-2 and Bax in the hepatic tissue of rats

2017 ◽  
Vol 95 (6) ◽  
pp. 708-713
Author(s):  
Mohammad Zamanian ◽  
Ali Shamsizadeh ◽  
Ali Esmaeili Nadimi ◽  
Mohammadreza Hajizadeh ◽  
Fatemeh Allahtavakoli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Muscle Fatigue ◽  
Biochemical Parameters ◽  
Hepatic Tissue ◽  
Control Group ◽  
Short Term ◽  
Sod Activity ◽  
Male Wistar Rats ◽  
Swimming Test ◽  
And Control

In the current study, the effects of troxerutin (TRX) on muscle fatigue and gene expression of Bcl-2 and Bax in the hepatic tissue of rats was investigated. Forty male Wistar rats were randomly divided into 4 groups and designated as control and TRX treatment at 75 (TRX75), 150 (TRX150), and 300 mg/kg per day (TRX300). The treated groups and control group received TRX and water orally for 7 days. After an exhaustive swimming test on the 7th day, all animals were euthanized immediately and several biochemical parameters related to fatigue and gene expression of Bcl-2 and Bax in the hepatic tissue were measured. Our results showed that the exhaustion swimming time in the TRX300 groups significantly increased 1.2-fold compared with the control group (P < 0.001). TRX300 significantly reduced ALT (P < 0.05) activity and increased liver SOD activity compared with the control group (P < 0.01). Additionally, TRX significantly reduced the liver mRNA expressions of Bax (P < 0.001) and increased the Bcl-2/Bax ratio (P < 0.001) compared with the control group. Based on our data, TRX possesses anti-apoptotic and hepatoprotective action following exhaustive swimming exercise.

Protective effect of green tea extract against cadmium-induced testicular damage in rats in respect of oxidant/antioxidant equilibrium and androgen production

2020 ◽  
Vol 21 (1) ◽  
pp. 31-35
Author(s):  
Basma El-Desoky ◽  
Shaimaa El-Sayed ◽  
El-Said El-Said
Keyword(s):  
Gene Expression ◽  
Single Dose ◽  
Green Tea ◽  
Serum Testosterone ◽  
Green Tea Extract ◽  
Male Rats ◽  
Controlled Study ◽  
Control Group ◽  
Testicular Damage ◽  
Tea Extract

Objective: Investigating the effect of green tea extract (GTE) on the testicular damage induced by cadmium chloride CdCl2 in male rats. Design: Randomized controlled study. Animals: 40 male Wistar rats. Procedures: Rats were randomly divided into four groups: A) control group (each rat daily received pellet diet); B) GTE group each rat daily received pellet diet as well as 3 ml of 1.5 % w/v GTE, C) CdCl2 group each rat was I/P injected a single dose of 1 mg/kg CdCl2, then daily received pellet diet, and D) CdCl2+GTE group each rat was I/P injected a single dose of 1 mg/kg CdCl2 then daily received pellet diet as well as 3 ml of 1.5 % w/v GTE. After 30 days, blood samples were collected for hormonal assays (testosterone, FSH, and LH). In addition, both testes were collected; one of them was used for quantification of 17-beta hydroxysteroid dehydrogenase III (17β-HSDIII) gene expression using a real-time PCR. The other testis was used for determination of catalase and reduced glutathione; GSH, Nitric oxide (NO) and malondialdehyde (MDA) levels. Results: CdCl2 decreased serum testosterone levels and its synthesis pathway (17β-HSDIII testicular gene expression). While antioxidants catalase and GSH were reduced, oxidants MDA were enriched in the testes of CdCl2-poisoned rats. This CdCl2-promoted testicular dysfunction was corrected via the administration of GTE to male rats. Conclusion and clinical relevance: GTE could be used as a remedy for protecting against CdCl2-induced testicular damage in male rats.

Mechanism Involved in Fortification by Berberine in CDDP-Induced Nephrotoxicity

2020 ◽  
Vol 13 (4) ◽  
pp. 342-352 ◽  
Author(s):  
Vipin K. Verma ◽  
Salma Malik ◽  
Ekta Mutneja ◽  
Anil K. Sahu ◽  
Kumari Rupashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Tissue ◽  
Isoquinoline Alkaloid ◽  
Experimental Models ◽  
Beclin 1 ◽  
Control Treatment ◽  
Control Group ◽  
Treatment Groups ◽  
Single Intraperitoneal Injection ◽  
Male Wistar Rats

Background: The activation of Nrf2/HO-1 pathway has been shown to protect against cisplatin- induced nephrotoxicity by reducing oxidative stress. Berberine (Ber), an isoquinoline alkaloid, has demonstrated antioxidant, anti-inflammatory and anti-apoptotic activities in various experimental models. Aim: To check the effect of Ber on cisplatin-induced nephrotoxicity and to explore the involved mechanism. Methods: Adult male Wistar rats were divided into 6 groups: Normal, cisplatin-control, treatment groups and per se group. Normal saline and Ber (20, 40 and 80 mg/kg; p.o.) was administered to rats for 10 days. A single intraperitoneal injection of cisplatin (8 mg/kg) was injected on 7th day to induced nephrotoxicity. On 10th day, rats were sacrificed, the kidney was removed and stored for the estimation of various parameters. Results: As compared to cisplatin-control group, Ber pretreatment improved renal function system and preserved renal architecture. It also diminished oxidative stress by upregulating the expression of Nrf2/HO-1 proteins. In addition, Ber attenuated the cisplatin mediated inflammation and apoptosis. Furthermore, it also reduced the phosphorylation of p38/JNK and PARP/Beclin-1 expression in the kidney. Conclusion: Ber attenuated renal injury by activating Nrf2/HO-1 and inhibiting JNK/p38MAPKs/ PARP/Beclin-1 expression which prevented oxidative stress, inflammation, apoptosis and autophagy in renal tissue.

scholarly journals Effect of Spirulina (Arthrospira platensis) on blood uric acid, hemoglobin and kidney histo-texture of mice treated with acetaminophen

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
M.` Zeenat ◽  
S. Sharmin ◽  
M. T. Islam ◽  
K. M. Sujan ◽  
M. I. Haque ◽  
...  
Keyword(s):  
Uric Acid ◽  
Uric Acid Level ◽  
Acid Level ◽  
Histopathological Examination ◽  
Research Work ◽  
Arthrospira Platensis ◽  
Renal Tissue ◽  
Diet Group ◽  
Normal Diet ◽  
Control Group

Background: Acetaminophen is a medication used to treat pain and fever. It is typically used for mild to moderate pain relief. Spirulina is a biomass of cyanobacteria that cultivated worldwide and used as a dietary supplement or whole food. It is also used as a feed supplement in the aquaculture, aquarium, and poultry industries. The present study was undertaken to determine the effect of Spirulina on blood and kidney in mice. Methods: Twenty Swiss Albino mice (Mus musculus) were randomly divided into 4 equal groups’ viz., A, B, C, and D. Group A was kept as control and fed only normal diet. Group B was supplemented with acetaminophen where as group C was supplemented with acetaminophen and Spirulina, and group D was treated with Spirulina. Results: The application of acetaminophen did not have significant effect on hemoglobin and uric acid content. But the addition of Spirulina to the diet increased significantly (P<0.05) hemoglobin and uric acid level. Histopathological examination revealed that no significant changes were found in the kidney of all of treated groups in comparison with the mice of control group. Conclusions: The research work suggests that long-term ingestion of acetaminophen does not exert a significant change in hemoglobin or uric acid level but spirulina supplemented diet may be associated with the rise in hemoglobin and uric acid level without affecting renal tissue texture in a significant manner.

scholarly journals Upregulation of Kiss-1 and Gpr54 Genes Expression in Pituitary of Male Rats Following the Central Administration of Neuropeptide Y

2019 ◽  
Vol 4 (4) ◽  
pp. 137-142
Author(s):  
Vahid Azizi ◽  
Shahrbanoo Oryan ◽  
Homayuon Khazali ◽  
Abdolkarim Hosseini
Keyword(s):  
Gene Expression ◽  
Pituitary Gland ◽  
Neuropeptide Y ◽  
Wistar Rats ◽  
Third Ventricle ◽  
Male Rats ◽  
Control Group ◽  
Central Administration ◽  
Reproductive Axis ◽  
Male Wistar Rats

Introduction: The neuropeptide Y (NPY) in the neural circuits of the hypothalamus has a stimulating effect on reproductive activities in mammals. Kisspeptin (KiSS1) is a quintessential neurotransmitter in the reproductive axis which directly stimulates gonadotropin-releasing hormone neurons in the hypothalamus. The distribution of KiSS1 expressing cells in the pituitary was described previously. Despite earlier reports showing the KiSS1 receptor, G-protein coupled receptor 54 (GPR54) expression in the pituitary, the potential physiological roles of kisspeptin at this gland have remained obscure. Accordingly, this study investigated the role of NPY on the relative expression of Kiss1 and Gpr54 genes in the pituitary gland in male Wistar rats. Methods: In general, 20 male Wistar rats weighing 200-250 g in 4 groups (5 in each group) received saline, NPY (2.3 nM), BIBP3226 (NPY receptor antagonist, 7.8 nM), and NPY+ BIBP3226. Then, they received the simultaneous injection of these molecules through the third ventricle of the brain. Finally, the relative mean expressions of Kiss1 and Gpr54 genes in the anterior pituitary were quantitatively analyzed by the real-time polymerase chain reaction. Results: The central injection of NPY increased the relative mean expressions of Kiss1 and Gpr54 genes in the pituitary gland compared to the control group although the injection of BIBP3226 eradicated these effects. However, the gene expression of Gpr54 in the rats receiving NPY coupled with BIBP3226 in hypophysis in comparison to the group receiving only NPY demonstrated a significant reduction (P<0.05). Conclusion: Overall, the central injection of NPY stimulated the gene expression of Kiss1 and Gpr54 in the pituitary gland.

Vitamin A deficiency regulates the expression of ferritin in young male Wistar rats

2021 ◽  
Vol 34 ◽  
Author(s):  
Mauricio RESTREPO-GALLEGO ◽  
Luis Eduardo DÍAZ ◽  
Juan David OSPINA-VILLA ◽  
Danny CHINCHILLA-CÁRDENAS
Keyword(s):  
Iron Deficiency ◽  
Vitamin A ◽  
Biochemical Parameters ◽  
Serum Iron ◽  
Wistar Rats ◽  
Vitamin A Deficiency ◽  
Young Male ◽  
Control Group ◽  
Transferrin Receptors ◽  
Male Wistar Rats

ABSTRACT Objective Iron deficiency and vitamin A deficiency are two of the main micronutrient deficiencies. Both micronutrients are essential for human life and children's development. This study aimed to investigate the effects of vitamin A deficiency on ferritin and transferrin receptors' expression and its relationship with iron deficiency. Methods Five diets with different vitamin A-to-iron ratios were given to thirty five 21-day-old male Wistar rats (separated in groups of seven animals each). The animals received the diet for six weeks before being euthanized. Serum iron and retinol levels were measured as biochemical parameters. Their duodenums, spleens, and livers were analyzed for the expression of ferritin and transferrin receptors by Western Blotting. Results Regarding biochemical parameters, the results show that when both vitamin A and iron are insufficient, the serum iron content (74.74µg/dL) is significantly lower than the control group (255.86µg/dL). The results also show that vitamin A deficiency does not influence the expression of the transferrin receptor, but only of the ferritin one. Conclusion Vitamin A deficiency regulates the expression of ferritin in young male Wistar rats.

scholarly journals P0690CORRELATIONS BETWEEN OPG/RANKL/RANK AXIS, VITAMIN D STATUS, PTH AND VASCULAR CALCIFICATION IN AN ADENINE-INDUCED MODEL OF CHRONIC KIDNEY DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Beata Sieklucka ◽  
Tomasz Domaniewski ◽  
Marta Zieminska ◽  
Malgorzata Galazyn-Sidorczuk ◽  
Anna Pawlak ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Control Group ◽  
Urea Nitrogen ◽  
And Control ◽  
Rank Gene

Abstract Background and Aims Chronic kidney disease (CKD) is a major public health problem worldwide and refers to a wide range of disorders in bone and mineral metabolism, abnormalities of biochemical parameters and pathological calcification of the blood vessels. Vascular calcification (VC) is a common complication in CKD patients, contributes to cardiovascular disease (CVD), and associates with increased mortality and morbidity. The precise mechanism of VC in CKD is not yet fully understood. Recently discovered molecules such as osteoprotegerin (OPG), its ligand receptor activator of nuclear factor NF-κB ligand (RANKL) and RANK are not only well-known to play a crucial role in bone homeostasis, but they has also been implicated in the process of development of vascular complications However the exact role of OPG/RANKL/RANK axis in the process of VC has not been yet fully assessed. Thus, the aim of this work is to evaluate the role of OPG/RANKL/RANK axis in the process of calcification in CKD. Method Seventy two male Wistar rats weighing 260-290 g (8-weeks old) were initially divided into 6 groups containing 12 animals in each group. Rats were divided into six groups: control rats (K4, K6, K8) and CKD rats (B4, B6, B8). Control group rats received standard diet, whereas CKD rats were fed a low adenine – diet containing 0.3 % adenine, 1.0 % Ca, 1.2 % Pi through 4 (K4, B4), 6 (K6, B6) and 8 (K8, B8) weeks. Subsequently, CKD and control rats were sacrificed at weeks 4 (n=24), 6 (n=24) and 8 (n=24). One day before being killed, the rats were placed in metabolic cages for 24-hour urine collection. Thereafter, the rats were anesthetized and samples of blood, as well as aortas were collected. Next, the OPG, RANKL, parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxy vitamin D3 1,25(OH)2D3 concentrations were determined using appropriate ELISA kits. Then the sRANKL/OPG ratio was calculated. The OPG, RANK and RANKL gene expression was assessed using real-time PCR (RT-PCR). The VC was quantified by measurement of the arterial calcium (Ca) and phosphate (Pi) content using flame atomic absorption. Serum levels of urea nitrogen, creatinine, uric acid, Ca, Pi and urinary levels of creatinine, Ca and Pi were measured. Results There was a progressive increase in serum urea nitrogen, creatinine, uric acid and PTH of CKD rats in comparison to control values. We also observed significantly decreased levels of 25(OH)D, 1,25(OH)2D and serum Ca. Total Ca content in the aorta was significantly increased in CKD rats in comparison with control group, whereas total Pi content in the aorta was significantly increased only in B8 group in comparison to appropriate controls. There were no differences in serum OPG and sRANKL levels between CKD and control rats. In contrast, we observed decreased OPG, RANKL and RANK gene expression in a B4 group in comparison to appropriate controls, whereas in a B6 group we noticed increased OPG, RANKL and decreased RANK gene expression. B8 group revealed increased RANKL and RANK gene expression, but there were no differences in OPG gene expression between CKD rats and control group. Furthermore, we observed positive correlations between serum sRANKL and OPG and RANK gene expression. Ca and P content in the aorta inversely corelated with RANKL gene expression, whereas positively with OPG gene expression. Serum 25(OH)D concentrations correlated inversely with Ca in aorta. PTH was positively correlated with serum RANKL and OPG and gene expression these cytokines. Conclusion Our results suggest that OPG/RANK/RANKL axis may be involved in the process of vascular calcification in chronic kidney disease. However, its role and evaluation of precise mechanism in this field requires further evaluation.

scholarly journals Thymoquinone Upregulates Catalase Gene Expression and Preserves the Structure of the Renal Cortex of Propylthiouracil-Induced Hypothyroid Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Nasra Ayuob ◽  
Maha Jameal Balgoon ◽  
Ahmed A. El-Mansy ◽  
Wafaa A. Mubarak ◽  
Alaa El-Din L. Firgany
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Protective Effect ◽  
Renal Cortex ◽  
Nigella Sativa ◽  
Serum Levels ◽  
Renal Tissue ◽  
Renal Diseases ◽  
Catalase Gene ◽  
Male Wistar Rats

Background. The association between hypothyroidism and renal diseases has been described in many studies. Nigella Sativa was among the recently reported natural product that has the potential to prevent renal tissue damage and fibrosis. The aim of this study was to evaluate the possible protective effect of thymoquinone on the structure of the renal cortex of hypothyroid rats and explore the mechanism behind it. Methods. An experimental model of hypothyroidism was induced in adult male Wistar rats by administration of propylthiouracil (6 mg/kg/body weight). One hypothyroid group was treated with thymoquinone at the dose of 50 mg/kg/body weight and compared to the untreated group. Thyroid function and oxidant/antioxidant status were assessed in the serum. Catalase gene expression was assessed using the real-time polymerase chain reaction. The kidney was assessed both histologically and immunohistochemically. Results. Administration of propylthiouracil resulted in a significant decrease in the serum levels of nitric oxide, reduced glutathione, and superoxide dismutase activity while the level of malondialdehyde significantly (p<0.001) increased. Administration of thymoquinone alleviated this effect on the thyroid hormones and significantly increased the serum levels of antioxidants. Thymoquinone significantly (p<0.001) upregulated catalase transcription by about 24-fold and could block the hypothyroidism-induced glomerular and tubular injury. Conclusion. Thymoquinone may have a potential protective effect against hypothyroidism-induced renal injury acting through the attenuation of the oxidative stress and upregulation of renal catalase gene expression.

scholarly journals Effects of Exposure to Aflatoxin G1 on the Plasma Biochemical Factors and Histopathological Properties of Renal Tissue in Mice

2021 ◽  
Vol 15 (2) ◽  
pp. 127-134
Author(s):  
Touraj Zamir-Nasta ◽  
◽  
Arash Ahmadi ◽  
Moein Yazdkhasti ◽  
Mona Pazhouhi ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Biochemical Analysis ◽  
Plasma Concentrations ◽  
Renal Tissue ◽  
Control Group ◽  
Male Mice ◽  
Blood Samples ◽  
Aquaporin 1 ◽  
Histopathological Studies ◽  
Sodium And Potassium

Background: Among aflatoxins, the subtype aflatoxin G1 is one of the most toxic, commonly found in cereals, legumes, dairy and non-alcoholic beers. Aflatoxins have been known as nephrotoxic compounds. In this study, changes in the expression of aquaporin-1, the histopathology of renal tissue and plasma biochemical factors after exposure to aflatoxin G1 were investigated in mice. Methods: Twenty-four adult male mice (weighing 20±2 g) were divided into four groups of six. The control group received the vehicle (0.2 ml) and the three experimental groups were injected intraperitoneally with aflatoxin G1 at 20 μg/kg for 7, 15 or 35 days, respectively. On days 7, 15 and 35, blood samples were drawn from the mice for biochemical analysis of plasma and the kidney tissues were sampled for real-time PCR and histopathological studies. Results: The real PCR results showed a reduction in aquaporin-1 expression in the experimental groups compared to those in the controls (P<0.05). Also, the plasma concentrations of urea and creatinine were significantly increased in the experimental groups compared to those in the controls (P<0.05). Also, the serum sodium and potassium levels had decreased significantly compared to the controls (P<0.05). Various damages were observed in the ureters and glomeruli among the experimental groups compared to those in the controls. Conclusion: Aflatoxin G1 had adverse effects on the renal tissue by reducing the expression of aquaporin-1. Subsequently, there were biochemical manifestations in the serum, consisting of changes in the concentrations of urea, creatinine, sodium and potassium, confirming the histopathological toxicity of aflatoxin G1.

scholarly journals Interaction Between Acute Exercise and Carnitine Supplementation on the Expression of Genes Involved in Liver Metabolism in Male Rats

2021 ◽  
Vol 12 (4) ◽  
pp. 4348-4356
Keyword(s):  
Gene Expression ◽  
Acute Exercise ◽  
Liver Metabolism ◽  
Male Rats ◽  
Control Group ◽  
Carnitine Supplementation ◽  
Serum Factors ◽  
Beneficial Effects ◽  
Expression Of Genes ◽  
Male Wistar Rats

Acute exercise induces rapid and dramatic induction of transcription in the liver. The beneficial effects of carnitine on serum factors and gene expression have been proven. This study examined the interaction between acute exercise and carnitine supplementation on the expression of genes involved in liver metabolism. Thirty-two male Wistar rats were randomly assigned into 4 groups (n = 8): Group 1 control, Group 2 received 200 mg/kg/day LCAR, Group 3 performed acute exercise, and Group 4 received LCAR and performed acute exercise. Gene expression in the liver was evaluated by Real-time PCR. Acute exercise significantly increased PDK4 expression compared to other groups. Also, carnitine administration, performing an acute exercise, and combination of LCAR-Acute significantly increased AMPK and PGC-1a expression compared with the control group. The expression of SREBP-1c and SCD1 was not significantly changed between studies. The combination of acute exercise and carnitine administration increased PGC-1a expression, indicating the importance of carnitine with exercise as a beneficial supplement.

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