The ethanol leaf extract of Andrographis paniculata blunts acute renal failure in cisplatin-induced injury in rats through inhibition of Kim-1 and upregulation of Nrf2 pathway

2018 ◽  
Vol 30 (2) ◽  
pp. 205-217 ◽  
Author(s):  
Bisi O. Adeoye ◽  
Ademola A. Oyagbemi ◽  
Ebunoluwa R. Asenuga ◽  
Temidayo O. Omobowale ◽  
Adeolu A. Adedapo
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Serum Creatinine ◽  
Leaf Extract ◽  
Histopathological Examination ◽  
Hematological Parameters ◽  
Kidney Tissue ◽  
Inflammatory Cells ◽  
Andrographis Paniculata ◽  
Markers Of Oxidative Stress

Abstract Background Cisplatin (CP) is a novel drug of choice in the treatment of cancer but its major limitation is nephrotoxicity, which is dose limiting. Andrographis paniculata (AP) is a common Indian dietary component. It is well known for its medicinal properties. This present study investigated the nephroprotective effect of ethanol leaf extract of Andrographis paniculata (EEAP) on CP-induced nephrotoxicity. Methods CP was used to induce nephrotoxicity in male Wistar rats to study the effect of EEAP on renal damages using hematological parameters, biochemical parameters, histology, and immunohistochemistry studies. Results The effects of EEAP were determined by CP-induced changes in different kidney tissue on antioxidant enzymes, markers of oxidative stress, serum creatinine, and urine parameters. Administration of EEAP (200 mL/kg and 400 mg/kg orally), prior to and following a single dose CP treatment (10 mg/kg i.p), significantly mitigated the CP-induced decrease in antioxidant enzymes, and increase in markers of oxidative stress, serum creatinine, and urinary protein. On histopathological examination of the kidney tissue, there was severe glomerular degeneration and infiltration of inflammatory cells in CP only treated rats, mild glomerular degeneration, and infiltration of inflammatory cells in EEAP pre-treated rats. Furthermore, EEAP activated Nrf2 and mitigated Kim-1 pathways in CP-induced nephrotoxicity. Conclusions The results showed the protective effect of EEAP against CP-induced nephrotoxicity.

The Protective Effect of the Ethanol Leaf Extract of Andrographis Paniculata on Cisplatin-Induced Acute Kidney Injury in Rats Through nrf2/KIM-1 Signalling Pathway

Drug Research ◽  
2017 ◽  
Vol 68 (01) ◽  
pp. 23-32 ◽  
Author(s):  
Bisi Adeoye ◽  
Ebunoluwa Asenuga ◽  
Ademola Oyagbemi ◽  
Temidayo Omobowale ◽  
Adeolu Adedapo
Keyword(s):  
Oxidative Stress ◽  
Normal Saline ◽  
Leaf Extract ◽  
Kidney Injury ◽  
Inflammatory Cells ◽  
Andrographis Paniculata ◽  
Stress Markers ◽  
Markers Of Oxidative Stress ◽  
Group B ◽  
Lower Expression

AbstractThe ethanol leaf extract of Andrographis paniculata was used to ameliorate the renal toxicity induced by cisplatin in 28 rats divided into four groups of seven rats per group. Group A received normal saline for the duration of the experiment. Group B animals were treated with cisplatin (10 mg/kg i.p) on day 1 and 3 days after received normal saline for the next 7 days while groups C and D animals also received 10 mg/kg dose of cisplatin on day 1 but after 3 days were then respectively treated with 200 and 400 mg/kg doses of the extract of Andrographis paniculata for the remaining 7 days through oral administration. Serum chemistry was used for the determination of markers of oxidative stress, anti-oxidant enzymes, serum biomarkers etc. Histopathology and immunohistochemistry were also carried out. Results showed that all oxidative stress markers assayed were significantly increased in group B animals but reverse is the case for groups C and D. On the other hand, antioxidant enzymes assayed experienced significant increase for groups C and D while these parameters experienced significant decrease for group B animals. Histopathology showed severe infiltration of inflammatory cells into renal tissues of group B animals whereas for groups C and D animals, only moderate glomerular degeneration was noted. In immunohistochemistry, while there is higher expression of KIM-1 for group B, there was a lower expression in groups C and D. Again, there was lower expression of Nrf2 for group B but higher expressions in groups C and D animals.

scholarly journals Effect of the French Oak Wood Extract Robuvit on Markers of Oxidative Stress and Activity of Antioxidant Enzymes in Healthy Volunteers: A Pilot Study

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Martina Horvathova ◽  
Zuzana Orszaghova ◽  
Lucia Laubertova ◽  
Magdalena Vavakova ◽  
Peter Sabaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Antioxidant Capacity ◽  
Healthy Volunteers ◽  
Total Antioxidant Capacity ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Total Antioxidant ◽  
Trolox Equivalent ◽  
Markers Of Oxidative Stress

We examinedin vitroantioxidant capacity of polyphenolic extract obtained from the wood of oakQuercus robur(QR), Robuvit, using TEAC (Trolox equivalent antioxidant capacity) method and the effect of its intake on markers of oxidative stress, activity of antioxidant enzymes, and total antioxidant capacity in plasma of 20 healthy volunteers. Markers of oxidative damage to proteins, DNA, and lipids and activities of Cu/Zn-superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were determined in the erythrocytes. We have found anin vitroantioxidant capacity of Robuvit of 6.37 micromole Trolox equivalent/mg of Robuvit. One month intake of Robuvit in daily dose of 300 mg has significantly decreased the serum level of advanced oxidation protein products (AOPP) and lipid peroxides (LP). Significantly increased activities of SOD and CAT as well as total antioxidant capacity of plasma after one month intake of Robuvit have been shown. In conclusion, we have demonstrated for the first time that the intake of Robuvit is associated with decrease of markers of oxidative stress and increase of activity of antioxidant enzymes and total antioxidant capacity of plasmain vivo.

scholarly journals Cardioprotective Potential of Polyphenolic Rich Green Combination in Catecholamine Induced Myocardial Necrosis in Rabbits

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Fatiqa Zafar ◽  
Nazish Jahan ◽  
Khalil-Ur-Rahman ◽  
Ahrar Khan ◽  
Waseem Akram
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Histopathological Examination ◽  
Cardiac Injury ◽  
Myocardial Necrosis ◽  
Myocardial Cell ◽  
Marker Enzymes ◽  
Cardiac Marker ◽  
Synthetic Drugs ◽  
Plant Mixture

The present study was designed to develop safer, effective, and viable cardioprotective herbal combination to control oxidative stress related cardiac ailments as new alternatives to synthetic drugs. The synergetic cardioprotective potential of herbal combination of four plantsT. arjuna(T.A.),P. nigrum(P.N),C. grandiflorus(C), andC. oxyacantha(Cr) was assessed through curative and preventive mode of treatment. In preventive mode of treatment, the cardiac injury was induced with synthetic catecholamine (salbutamol) to pretreated rabbits with the proposed herbal combination for three weeks. In curative mode of treatment, cardiotoxicity/oxidative stress was induced in rabbits with salbutamol prior to treating them with plant mixture. Cardiac marker enzymes, lipids profile, and antioxidant enzymes as biomarker of cardiotoxicity were determined in experimental animals. Rabbits administrated with mere salbutamol showed a significant increase in cardiac marker enzymes and lipid profile and decrease in antioxidant enzymes as compared to normal control indicating cardiotoxicity and myocardial cell necrosis. However, pre- and postadministration of plant mixture appreciably restored the levels of all biomarkers. Histopathological examination confirmed that the said combination was safer cardioprotective product.

Mancozeb induces testicular dysfunction through oxidative stress and apoptosis: Protective role of N-acetylcysteine antioxidant

2018 ◽  
Vol 34 (11) ◽  
pp. 798-811 ◽  
Author(s):  
Mohaddeseh Mohammadi-Sardoo ◽  
Ali Mandegary ◽  
Mohammad Nabiuni ◽  
Seyed-Noureddin Nematollahi-Mahani ◽  
Bagher Amirheidari
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Reproductive System ◽  
Histopathological Examination ◽  
Antioxidant Property ◽  
Testicular Tissue ◽  
Protective Role ◽  
Protein Carbonyl ◽  
Mrna Levels ◽  
Nadph Oxidase 4

Mancozeb (MZB) is one of the fungicides used in pest control programs that might affect human health including reproductive system. The aim of this study was to demonstrate the mechanisms through which MZB induces testicular tissue damage and the probable protective effect of N-acetylcysteine (NAC), a modified amino acid, with antioxidant property, against MZB toxicity in an animal model. Male albino mice ( n = 8) were exposed to different doses of MZB (250 and 500 mg/kg/day) by oral gavage without or with NAC (200 mg/kg, twice/week) for 40 days. Sub-chronic MZB dose-dependently decreased sperm motility and count. Exposure to MZB increased lipid peroxidation and protein carbonyl, while it reduced antioxidant enzymes activities, total antioxidant capacity, and glutathione content. The histopathological examination clearly showed deleterious changes in the testicular structure. At the molecular levels, the results of quantitative real time-poly chain reaction (qRT-PCR) showed that MZB upregulated oxidative stress markers inducible nitric oxide synthase (iNOS) and NADPH oxidase 4 (NOX4) and downregulated expression of the glutathione peroxidase 1 (Gpx1) gene as one of the most important antioxidant enzymes. MZB also induced apoptosis dose-dependently in the testes as determined by the terminal dUTP nick-end labeling assay and immunoblotting. NAC administration decreased the mRNA levels of both iNOS and NOX4 with a concomitant increase in Gpx1 expression. It also significantly decreased MZB-induced oxidative stress and apoptosis. Collectively, the present study showed MZB-induced oxidative damage in testes leading to apoptosis. It revealed that antioxidants such as NAC can mitigate oxidant injury induced by the dithiocarbamate pesticides in the reproductive system.

scholarly journals Treatment with pyrrolidine dithiocarbamate improves proteinuria, oxidative stress, and glomerular hypertension in overload proteinuria

2008 ◽  
Vol 295 (5) ◽  
pp. F1431-F1439 ◽  
Author(s):  
Edilia Tapia ◽  
Dolores J. Sánchez-González ◽  
Omar N. Medina-Campos ◽  
Virgilia Soto ◽  
Carmen Ávila-Casado ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Inflammatory Cell ◽  
Pyrrolidine Dithiocarbamate ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Glomerular Hypertension ◽  
Markers Of Oxidative Stress ◽  
Glomerular Hemodynamics ◽  
Reduced Activity

We evaluated whether the blockade of the proinflammatory transcription factor NF-κB would modify the oxidative stress, inflammation, and structural and hemodynamic alterations found in the kidney as a result of massive proteinuria. Twenty male Sprague-Dawley rats were injected with 2 g of BSA intraperitoneally daily for 2 wk. Ten of them received in addition the inhibitor of NF-κB activation pyrrolidine dithiocarbamate (PDTC; 200 mg·kg−1·day−1 sc) and the rest received vehicle. Seven rats that received intraperitoneal saline were used as controls. Glomerular hemodynamics were studied after 14 days. Markers of oxidative stress (NF-κB subunit p65+ cells, 3-nitrotyrosine, and 4-hydroxynonenal), inflammation (cortical CD68+ cells and NOS-II), and afferent arteriole damage were assessed by immunohistochemistry and morphometry. Activity of antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase was evaluated in renal cortex and medulla. Albumin overload induced massive proteinuria, oxidative stress with reduced activity of antioxidant enzymes, NF-κB activation, inflammatory cell infiltration, a significant presence of proteinaceous casts, systemic and glomerular hypertension, as well as arteriolar remodeling. Treatment with PDTC prevented or improved all of these findings. In this model of nephrotic syndrome, we demonstrate a key role for oxidative stress and inflammation in causing systemic and glomerular hypertension and proteinuria. Oxidative stress and inflammation may have a key role in accelerating renal injury associated with intense proteinuria.

The biochemical effects of occupational exposure to lead and cadmium on markers of oxidative stress and antioxidant enzymes activity in the blood of glazers in tile industry

2018 ◽  
Vol 34 (7) ◽  
pp. 459-467 ◽  
Author(s):  
Maryam Hormozi ◽  
Ramazan Mirzaei ◽  
Alireza Nakhaee ◽  
Shahrokh Izadi ◽  
Javid Dehghan Haghighi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Occupational Exposure ◽  
Control Group ◽  
Blood Levels ◽  
Biochemical Effects ◽  
Lead And Cadmium ◽  
Total Antioxidant ◽  
Markers Of Oxidative Stress

The aim of the present study was to evaluate the effects of occupational exposure to lead (Pb) and cadmium (Cd) on markers of oxidative stress in glazers in tile industries. Total antioxidant capacity (TAC), malondialdehyde (MDA), and the activity of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were determined in the blood of 80 subjects, including 40 glazers and 40 nonexposed subjects. Mean levels of blood Cd (8.90 ± 2.80 µg/L) and blood Pb (62.90 ± 38.10 µg/L) of glazers showed a significant increase compared with the control group. In the serum of glazers, the level of MDA was significantly higher and the level of TAC was significantly lower than the control group. We have noted a disturbance in the levels of antioxidants by a significant increase in the CAT activity and a significant decrease in the activities of SOD and GPx in the serum of glazers compared with the controls. Correlation analysis demonstrated that the serum MDA level and CAT activity were positively associated with the blood levels of Pb and Cd. Also, GPx and SOD were negatively correlated with blood Cd levels. The study clearly indicated that co-exposure to Cd and Pb can induce oxidative stress in glazers, resulting in increased lipid peroxidation and altered antioxidant enzymes.

scholarly journals Phenolic Acids (Gallic and Tannic Acids) Modulate Antioxidant Status and Cisplatin Induced Nephrotoxicity in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Seun F. Akomolafe ◽  
Ayodele J. Akinyemi ◽  
Scholarstical O. Anadozie
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Body Weight ◽  
Gallic Acid ◽  
Tannic Acid ◽  
Histopathological Examination ◽  
Kidney Tissue ◽  
Control Group ◽  
Preventive Strategy ◽  
Oxidative Stress Biomarkers

Cisplatin (cis-diamminedichloroplatinum (II) or CDDP), used in the treatment of many solid-tissue cancers, has its chief side-effect in nephrotoxicity. Hence, this study sought to investigate and compare the protective effect of gallic acid (GA) and tannic acid (TA) against cisplatin induced nephrotoxicity in rats. The rats were given a prophylactic treatment of GA and TA orally at a dose of 20 and 40 mg/kg body weight for 7 consecutive days before the administration of a single intraperitoneal (i.p.) injection of cisplatin (CP) at 7.5 mg/kg bwt. The protective effects of both GA and TA on CP induced nephrotoxicity were investigated by assaying renal function, oxidative stress biomarkers, and histopathological examination of kidney architecture. A single dose of cisplatin (7.5 mg/kg bwt) injected i.p. caused a significant increase in some biomarkers of renal function (creatinine, uric acid, and urea levels), with a marked elevation in malondialdehyde (MDA) content accompanied by a significant (P<0.05) decrease in reduced glutathione (GSH) content (103.27%) of kidney tissue as compared to control group. Furthermore, a significant (P<0.05) reduction in kidney antioxidant enzymes (SOD, catalase, GPx, and GST) activity was observed. However, pretreatment with oral administration of tannic acid and gallic acid at a dose of 20 and 40 mg/kg body weight, respectively, for 7 days prior to cisplatin administration reduced histological renal damage and suppressed the generation of ROS, lipid peroxidation, and oxidative stress in kidney tissues. These results indicate that both gallic and tannic acids could serve as a preventive strategy against cisplatin induced nephrotoxicity.

scholarly journals Manganese-Induced Nephrotoxicity Is Mediated through Oxidative Stress and Mitochondrial Impairment

2020 ◽  
Vol 4 (2) ◽  
pp. 1-10 ◽  
Author(s):  
Amir Mohammad Niknahad ◽  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Leila Moezi ◽  
Reza Heidari
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Essential Element ◽  
The Other ◽  
Tubular Atrophy ◽  
Mitochondrial Impairment ◽  
Other Hand ◽  
Markers Of Oxidative Stress ◽  
Dehydrogenases Activity

Manganese (Mn) is an essential element that is incorporated in various metabolic pathways and enzyme structures. On the other hand, a range of adverse effects has been described in association with Mn overexposure. Mn is a well-known neurotoxic agent in mammals. Renal injury is another adverse effect associated with Mn intoxication. No precise mechanism for Mn nephrotoxicity has been identified so far. The current study was designed to evaluate the potential mechanisms of Mn-induced renal injury. Rats were treated with Mn (20 and 40 mg/mL, respectively, in drinking water) for 30 consecutive days. Markers of oxidative stress, as well as several mitochondrial indices, were assessed in the kidney tissue. Renal injury was evident in Mn-treated animals, as judged by a significant increase in serum BUN and creatinine. Moreover, urinalysis revealed a significant increase in urine glucose, phosphate, and protein in Mn-treated rats. Kidney histopathological alterations, including tubular atrophy, interstitial inflammation, and necrosis, were also detected in Mn-treated animals. Biomarkers of oxidative stress, including an increment in reactive oxygen species (ROS), lipid peroxidation, and oxidized glutathione (GSSG), were detected in Mn-treated groups. On the other hand, kidney glutathione (GSH) stores and total antioxidant capacity were depleted in Mn groups. Mn exposure was associated with significant mitochondrial depolarization, decreased mitochondrial dehydrogenases activity, mitochondrial permeabilization, and depletion of adenosine tri-phosphate (ATP) content. These data highlight oxidative stress and mitochondrial impairment as potential mechanisms involved in Mn-induced renal injury.

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