Dietary exposure to silver nanoparticles in Sprague–Dawley rats: Effects on oxidative stress and inflammation

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene, with subsequent elevated tissue ANG II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5–8 g of glomerular filtered albumin each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of ANG II-induced oxidative stress in PTC structural remodeling: whether such changes could be modified with in vivo treatment with ANG type 1 receptor (AT1R) blockade (valsartan) or SOD/catalase mimetic (tempol). Male Ren2 (6–7 wk old) and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Systolic blood pressure, albuminuria, N-acetyl-β-d-glucosaminidase, and kidney tissue malondialdehyde (MDA) were measured, and ×60,000 transmission electron microscopy images were used to assess PTC microvilli structure. There were significant differences in systolic blood pressure, albuminuria, lipid peroxidation (MDA and nitrotyrosine staining), and PTC structure in Ren2 vs. Sprague-Dawley rats (each P < 0.05). Increased mean diameter of PTC microvilli in the placebo-treated Ren2 rats ( P < 0.05) correlated strongly with albuminuria ( r2 = 0.83) and moderately with MDA ( r2 = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in placebo-treated Ren2 rats compared with Sprague-Dawley control rats ( P < 0.05). AT1R blockade, but not tempol treatment, abrogated albuminuria and N-acetyl-β-d-glucosaminidase; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to the oxidative stress response to ANG II and/or albuminuria.

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Effect of liposome-encapsulated hemoglobin resuscitation on proteostasis in small intestinal epithelium after hemorrhagic shock

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00157.2016 ◽

2016 ◽

Vol 311 (1) ◽

pp. G180-G191 ◽

Cited By ~ 2

Author(s):

Geeta Rao ◽

Vivek R. Yadav ◽

Shanjana Awasthi ◽

Pamela R. Roberts ◽

Vibhudutta Awasthi

Keyword(s):

Oxidative Stress ◽

Hemorrhagic Shock ◽

Multiorgan Failure ◽

Sprague Dawley ◽

Barrier Dysfunction ◽

Protective Mechanisms ◽

Unfolded Protein ◽

Sprague Dawley Rats ◽

Markers Of Oxidative Stress ◽

Protein Response

Gut barrier dysfunction is the major trigger for multiorgan failure associated with hemorrhagic shock (HS). Although the molecular mediators responsible for this dysfunction are unclear, oxidative stress-induced disruption of proteostasis contributes to the gut pathology in HS. The objective of this study was to investigate whether resuscitation with nanoparticulate liposome-encapsulated hemoglobin (LEH) is able to restore the gut proteostatic mechanisms. Sprague-Dawley rats were recruited in four groups: control, HS, HS+LEH, and HS+saline. HS was induced by withdrawing 45% blood, and isovolemic LEH or saline was administered after 15 min of shock. The rats were euthanized at 6 h to collect plasma and ileum for measurement of the markers of oxidative stress, unfolded protein response (UPR), proteasome function, and autophagy. HS significantly increased the protein and lipid oxidation, trypsin-like proteasome activity, and plasma levels of IFNγ. These effects were prevented by LEH resuscitation. However, saline was not able to reduce protein oxidation and plasma IFNγ in hemorrhaged rats. Saline resuscitation also suppressed the markers of UPR and autophagy below the basal levels; the HS or LEH groups showed no effect on the UPR and autophagy. Histological analysis showed that LEH resuscitation significantly increased the villus height and thickness of the submucosal and muscularis layers compared with the HS and saline groups. Overall, the results showed that LEH resuscitation was effective in normalizing the indicators of proteostasis stress in ileal tissue. On the other hand, saline-resuscitated animals showed a decoupling of oxidative stress and cellular protective mechanisms.

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Enteral Baicalin, a Flavone Glycoside, Reduces Indicators of Cardiac Surgery-Associated Acute Kidney Injury in Rats

Cardiorenal Medicine ◽

10.1159/000492159 ◽

2018 ◽

Vol 9 (1) ◽

pp. 31-40 ◽

Cited By ~ 3

Author(s):

Jing Shi ◽

Guofeng Wu ◽

Xiaohua Zou ◽

Ke Jiang

Keyword(s):

Oxidative Stress ◽

Acute Kidney Injury ◽

Cardiac Surgery ◽

Kidney Injury ◽

Renal Tissue ◽

Myeloperoxidase Activity ◽

Protective Effects ◽

Sprague Dawley ◽

Injury Index ◽

Sprague Dawley Rats

Background/Aims: Cardiac surgery-associated acute kidney injury (CSA-AKI) is one of the most common postoperative complications in intensive care medicine. Baicalin has been shown to have anti-inflammatory and antioxidant roles in various disorders. We aimed to test the protective effects of baicalin on CSA-AKI using a rat model. Methods: Sprague-Dawley rats underwent 75 min of cardiopulmonary bypass (CPB) with 45 min of cardioplegic arrest (CA) to establish the AKI model. Baicalin was administered at different doses intragastrically 1 h before CPB. The control and treated rats were subjected to the evaluation of different kidney injury index and inflammation biomarkers. Results: Baicalin significantly attenuated CPB/CA-induced AKI in rats, as evidenced by the lower levels of serum creatinine, serum NGAL, and Kim1. Baicalin remarkably inhibited oxidative stress, reflected in the decreased malondialdehyde and myeloperoxidase activity, and enhanced superoxide dismutase activity and glutathione in renal tissue. Baicalin suppressed the expression of IL-18 and iNOS, and activated the Nrf2/HO-1 pathway. Conclusion: Our data indicated that baicalin mediated CPB/CA-induced AKI by decreasing the oxidative stress and inflammation in the renal tissues, and that baicalin possesses the potential to be developed as a therapeutic tool in clinical use for CSA-AKI.

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Comparative and Combinatorial Effects of Resveratrol and Sacubitril/Valsartan alongside Valsartan on Cardiac Remodeling and Dysfunction in MI-Induced Rats

Molecules ◽

10.3390/molecules26165006 ◽

2021 ◽

Vol 26 (16) ◽

pp. 5006

Author(s):

Pema Raj ◽

Karen Sayfee ◽

Mihir Parikh ◽

Liping Yu ◽

Jeffrey Wigle ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiac Remodeling ◽

Left Ventricular ◽

Myocardial Tissue ◽

Additive Effects ◽

Sprague Dawley ◽

Neutrophil Gelatinase Associated Lipocalin ◽

Sprague Dawley Rats ◽

And Function ◽

Neutrophil Gelatinase

The development and progression of heart failure (HF) due to myocardial infarction (MI) is a major concern even with current optimal therapy. Resveratrol is a plant polyphenol with cardioprotective properties. Sacubitril/valsartan is known to be beneficial in chronic HF patients. In this study, we investigated the comparative and combinatorial benefits of resveratrol with sacubitril/valsartan alongside an active comparator valsartan in MI-induced male Sprague Dawley rats. MI-induced and sham-operated animals received vehicle, resveratrol, sacubitril/valsartan, valsartan alone or sacubitril/valsartan + resveratrol for 8 weeks. Echocardiography was performed at the endpoint to assess cardiac structure and function. Cardiac oxidative stress, inflammation, fibrosis, brain natriuretic peptide (BNP), creatinine and neutrophil gelatinase associated lipocalin were measured. Treatment with resveratrol, sacubitril/valsartan, valsartan and sacubitril/valsartan + resveratrol significantly prevented left ventricular (LV) dilatation and improved LV ejection fraction in MI-induced rats. All treatments also significantly reduced myocardial tissue oxidative stress, inflammation and fibrosis, as well as BNP. Treatment with the combination of sacubitril/valsartan and resveratrol did not show additive effects. In conclusion, resveratrol, sacubitril/valsartan, and valsartan significantly prevented cardiac remodeling and dysfunction in MI-induced rats. The reduction in cardiac remodeling and dysfunction in MI-induced rats was mediated by a reduction in cardiac oxidative stress, inflammation and fibrosis.

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The effect of Vitamin C on amodiaquine‐induced oxidative stress in the ovary of Sprague‐Dawley rats

The FASEB Journal ◽

10.1096/fasebj.27.1_supplement.743.7 ◽

2013 ◽

Vol 27 (S1) ◽

Author(s):

Stella C Gbotolorun ◽

Abraham A Osinubi ◽

Ademola A Oremosu ◽

Cressie C Noronha ◽

Amabe o Akpantah ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin C ◽

Sprague Dawley ◽

Sprague Dawley Rats

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Effects of Lead Nitrate Induced Histological Changes in Liver of Male Sprague Dawley Rats

10.53350/pjmhs2115112948 ◽

2021 ◽

Vol 15 (11) ◽

pp. 2948-2950

Author(s):

Sumaira Abbasi ◽

Mushtaq Ahmad ◽

Kaukab Anjum ◽

Amaidah Mir ◽

Ayesha Irfan ◽

...

Keyword(s):

Oxidative Stress ◽

Free Radicals ◽

Lead Nitrate ◽

Normal Diet ◽

The Body ◽

Central Vein ◽

Sprague Dawley ◽

Toxic Agent ◽

Sprague Dawley Rats ◽

Group B

Lead is a highly toxic agent and a potent risk factor for various diseases as its quantity in an environment is increasing day by day. Aim: To observe and analyze the lead nitrate induced histomorphological changes in the liver of Sprague Dawley rats. Study Design: Experimental Study. Methodology: Animals of group A (control) were fed on normal diet but the animals of group B were given 50mg/kg of lead nitrate dissolved in 10ml of distilled water through oral gavage for 14 days daily. SPSS version 22 was used for data analysis. All the quantitative data was expressed as means ± SD. One Way ANOVA followed by Post Hoc Tukey test was applied. Results: Degenerative effects were noted. The number of Inflammatory and Kupfffer cells is increased with decreased in the body weight. Steatosis and central vein congestion were also present. Conclusion: It was concluded that degenerative effects histologically may be due to oxidative stress produced by formation of free radicals and denaturation of proteins by lead nitrate. Keywords: Lead, Liver, Central Vein Congestion, Oxidative Stress and Free Radicals.

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ANTIOXIDANT AND ANTI-INFLAMMATORY EFFECTS OF CURCUMIN CONTRIBUTE INTO ATTENUATION OF ACUTE GENTAMICIN-INDUCED NEPHROTOXICITY IN RATS

Asian Journal of Pharmaceutical and Clinical Research ◽

10.22159/ajpcr.2019.v12i3.30875 ◽

2019 ◽

pp. 466-468 ◽

Cited By ~ 3

Author(s):

HAYDER M AL-KURAISHY ◽

ALI I AL-GAREEB ◽

HUDA ABDULBAKI RASHEED

Keyword(s):

Oxidative Stress ◽

Serum Creatinine ◽

Cystatin C ◽

Kidney Injury ◽

Specific Situation ◽

Distilled Water ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Group 2 ◽

Nephroprotective Effect

Objectives: Nephrotoxicity is a renal-specific situation in which the excretion of toxic metabolites is reduced due to toxic agents and drugs. Gentamicin is an antibiotic belongs to aminoglycoside group which may induce nephrotoxicity due to induction of oxidative stress. Curcumin is a component of traditional medicine with significant nephroprotective effect. Therefore, the objective of the present study was to evaluate the nephroprotective effect of curcumin on gentamicin-induced nephrotoxicity. Methods: A total of 30 male Sprague-Dawley rats were used which divided into Group 1 (n=10): Rats treated with distilled water 5 ml/kg plus normal saline 5 ml/kg for 12 days, Group 2 (n=10): Rats treated with distilled water 5 ml/kg plus gentamicin 100 mg/kg for 12 days, and Group 3 (n=10): Rats treated with curcumin 100 mg/kg plus gentamicin 100 mg/kg for 12 days. Blood urea, serum creatinine, malondialdehyde (MDA), kidney injury molecule (KIM-1), and cystatin-C were measured in both control and experimental groups. Results: Rats treated with gentamicin showed nephrotoxicity as evident by significant elevation in blood urea, serum creatinine, KIM-1, MDA, and cystatin-C sera levels. Curcumin leads to significant reduction of blood urea and serum creatinine compared to gentamicin group, p<0.05. Curcumin also reduced MDA, KIM-1, and cystatin-C sera levels significantly compared to gentamicin group, p<0.01. Conclusion: Curcumin produced significant nephroprotective effect on gentamicin-induced nephrotoxicity through modulation of oxidative stress and inflammatory biomarkers.

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