HO-1 induction attenuates renal damage and oxidative stress induced by K2Cr2O7

Background: Commonly used aminoglycosides have frequent side effect of nephrotoxicity, still are preferred by clinicians because of efficacy against gram negative bacteria, resistant bacteria, nosocomial infections and cost effectiveness. Gentamicin produces oxidative stress; substances ameliorating stress are used to reduce toxicity. Turmeric has multiple medicinal properties including potent antioxidant activity, hence study was undertaken.Methods: Eight groups containing six animals in each group, treated for 15 days. First group treated with normal saline. Second, fourth and sixth group treated with only gentamicin- sacrificed at 16, 22, 29th day. Third, fifth and seventh group treated with gentamicin and turmeric simultaneously and sacrificed on 16, 22, 29th day. Eighth group was pre-treated with turmeric for thirty days and concurrently treated with gentamicin and turmeric for 15 days and sacrificed on 16th day. Levels of blood urea, serum creatinine, superoxide dismutase and histopathological grades were assessed each time.Results: Severe renal dysfunction (146 ± 9.2, 2.03 ± 0.26), highest renal injury grading (3.66 ± 0.24) was observed in only gentamicin treated groups followed by spontaneous recovery after withdrawal of drug but with higher levels of oxidative stress (0.04 ± 0.01). Gentamicin and Turmeric treated groups maintained renal function and had lower level of renal damage grades and oxidative stress. Turmeric pre-treated group was having lowest oxidative stress (0.12 ± 0.03), histopathology grade (0.60 ± 0.06) with normal renal functions.Conclusions: Turmeric has potent antioxidant property which effectively protects kidney from damage induced because of gentamicin.

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Neutrophil Infiltration and Oxidative Stress May Play a Critical Role in Methotrexate-Induced Renal Damage

Chemotherapy ◽

10.1159/000192391 ◽

2009 ◽

Vol 55 (2) ◽

pp. 83-90 ◽

Cited By ~ 37

Author(s):

Viswa Kalyan Kolli ◽

Premila Abraham ◽

Bina Isaac ◽

Dhayakani Selvakumar

Keyword(s):

Oxidative Stress ◽

Renal Damage ◽

Critical Role ◽

Neutrophil Infiltration ◽

And Oxidative Stress

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Effect of Quamoclit angulata Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice

Antioxidants ◽

10.3390/antiox9060459 ◽

2020 ◽

Vol 9 (6) ◽

pp. 459 ◽

Cited By ~ 2

Author(s):

Ji Eun Park ◽

Heaji Lee ◽

Hyunkyung Rho ◽

Seong Min Hong ◽

Sun Yeou Kim ◽

...

Keyword(s):

Oxidative Stress ◽

Nlrp3 Inflammasome ◽

High Fat Diet ◽

Renal Damage ◽

Model Assessment ◽

Diabetic Mice ◽

Homeostasis Model Assessment ◽

And Oxidative Stress ◽

Type 2 Diabetic

Type 2 diabetes mellitus (T2DM) is caused by abnormalities of controlling blood glucose and insulin homeostasis. Especially, hyperglycemia causes hyper-inflammation through activation of NLRP3 inflammasome, which can lead to cell apoptosis, hypertrophy, and fibrosis. Quamoclit angulata (QA), one of the annual winders, has been shown ameliorative effects on diabetes. The current study investigated whether the QA extract (QAE) attenuated hyperglycemia-induced renal inflammation related to NLRP inflammasome and oxidative stress in high fat diet (HFD)-induced diabetic mice. After T2DM was induced, the mice were treated with QAE (5 or 10 mg/kg/day) by gavage for 12 weeks. The QAE supplementation reduced homeostasis model assessment insulin resistance (HOMA-IR), kidney malfunction, and glomerular hypertrophy in T2DM. Moreover, the QAE treatment significantly attenuated renal NLRP3 inflammasome dependent hyper-inflammation and consequential renal damage caused by oxidative stress, apoptosis, and fibrosis in T2DM. Furthermore, QAE normalized aberrant energy metabolism (downregulation of p-AMPK, sirtuin (SIRT)-1, and PPARγ-coactivator α (PGC-1 α)) in T2DM mice. Taken together, the results suggested that QAE as a natural product has ameliorative effects on renal damage by regulation of oxidative stress and inflammation in T2DM.

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Syzygium aromaticum Reduces Diabetes-induced Glucotoxicity via the NRF2/Glo1 Pathway

Planta Medica ◽

10.1055/a-1203-0452 ◽

2020 ◽

Vol 86 (12) ◽

pp. 876-883

Author(s):

Moon Ho Do ◽

Jiwon Choi ◽

Yoonsook Kim ◽

Sang Keun Ha ◽

Guijae Yoo ◽

...

Keyword(s):

Oxidative Stress ◽

Renal Damage ◽

Treated Group ◽

Diabetic Rats ◽

Related Factor ◽

Syzygium Aromaticum ◽

Inhibitory Effects ◽

Collagen Crosslinks ◽

Glycation End Products ◽

And Oxidative Stress

AbstractAdvanced glycation end products and methylglyoxal are known to show increased levels in diabetic conditions and induce diverse metabolic disorders. However, the antiglycation ability of the bark of Syzygium aromaticum is not yet studied. In this study, we determined the inhibitory effects of S. aromaticum on AGE formation. Moreover, S. aromaticum showed breakage and inhibitory ability against the formation of AGE-collagen crosslinks. In SV40 MES13 cells, treatment with the S. aromaticum extract significantly ameliorated MG-induced oxidative stress as well as cytotoxicity. Furthermore, in the S. aromaticum extract-treated group, there was a reduction in levels of several diabetic markers, such as blood glucose, kidney weight, and urinary albumin to creatinine ratio in streptozotocin-induced diabetic rats. Treatment with the S. aromaticum extract significantly increased the expression of nuclear factor erythroid 2-related factor 2, a transcription factor involved in the expression of antioxidant enzymes. Moreover, the treatment significantly upregulated the expression of glyoxalase 1 and downregulated the expression of receptor for AGEs. These results suggest that the S. aromaticum extract might ameliorate diabetes-induced renal damage by inhibiting the AGE-induced glucotoxicity and oxidative stress through the Nrf2/Glo1 pathway.

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Nephroprotective effect of silymarin against diclofenac induced renal damage and oxidative stress in male rats

Journal of Herbmed Pharmacology ◽

10.15171/jhp.2019.23 ◽

2019 ◽

Vol 8 (2) ◽

pp. 146-152 ◽

Cited By ~ 7

Author(s):

Ali Nouri ◽

Esfandiar Heidarian

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Vitamin C ◽

Group Treatment ◽

Renal Damage ◽

Male Rats ◽

Tissue Homogenate ◽

Control Group ◽

Tnf Α ◽

And Oxidative Stress

Introduction: Diclofenac (DIC), a phenylacetic acid compound which belongs to nonsteroidal anti-inflammatory drugs (NSAIDs), is generally used for the treatment of various diseases such as rheumatoid arthritis, ankylosing spondylitis, acute muscle pain conditions and osteoarthritis. Overdose of DIC can lead to renal injuries in both experimental animal and human. Our research was done to assess the protective role of silymarin on renal damage induced by DIC in rats. Methods: Thirty-two Wistar rats were assigned to four groups (n=8/group). Group 1 was control group; animals in group 2 were administrated DIC; Groups 3 and 4 administrated DIC plus silymarin with doses of 100 mg/kg and 200 mg/kg, orally (p.o), respectively. Various biochemical, molecular, and histological parameters were evaluated in serum and tissue homogenate. Results: In the second group, the levels of kidney catalase (CAT), vitamin C and superoxide dismutase (SOD) remarkably reduced (P < 0.05) relative to the control group. Also, urea, creatinine (Cr), malondialdehyde (MDA), serum tumor necrosis factor-α (TNF-α) and gene expression of TNF-α in this group were noticeably elevated (P < 0.05) relative to the control group. Treatment with silymarin caused a remarkable elevation (P < 0.05) in vitamin C, SOD, CAT and a remarkable reduction (P < 0.05) in the content of MDA, urea, Cr, TNF-α gene expression and serum TNF-α in comparison with second group. Histological injuries were also ameliorated by silymarin administration. Conclusion: The results confirm that silymarin has an ameliorative role against renal damage and oxidative stress induced by DIC in male rats.

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Association of renal damage and oxidative stress in a rat model of metabolic syndrome. Influence of gender

Free Radical Research ◽

10.1080/10715760903045296 ◽

2009 ◽

Vol 43 (8) ◽

pp. 761-771 ◽

Cited By ~ 47

Author(s):

Israel Pérez-Torres ◽

Priscilla Roque ◽

Mohammed El Hafidi ◽

Eulises Diaz-Diaz ◽

Guadalupe Baños

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Rat Model ◽

Renal Damage ◽

And Oxidative Stress

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Superoxide dismutase and oxidative stress in Dahl salt-sensitive and -resistant rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00346.2001 ◽

2002 ◽

Vol 283 (3) ◽

pp. R732-R738 ◽

Cited By ~ 104

Author(s):

Shumei Meng ◽

L. Jackson Roberts ◽

Garrick W. Cason ◽

Travis S. Curry ◽

R. Davis Manning

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Urinary Excretion ◽

Renal Damage ◽

Urinary Protein Excretion ◽

Urinary Protein ◽

Superoxide Production ◽

Protein Excretion ◽

Salt Sensitive Hypertension ◽

And Oxidative Stress

The roles of oxidative stress and renal superoxide dismutase (SOD) levels and their association with renal damage were studied in Dahl salt-sensitive (S) and salt-resistant (R)/Rapp strain rats during changes in Na intake. After 3 wk of a high (8%)-Na diet in S rats, renal medullary Cu/Zn SOD was 56% lower and Mn SOD was 81% lower than in R high Na-fed rats. After 1, 2, and 3 wk of high Na, urinary excretion of F2-isoprostanes, an index of oxidative stress, was significantly greater in S rats compared with R rats. Plasma F2-isoprostane concentration increased in the 2-wk S high Na-fed group. After 3 wk, renal cortical and medullary superoxide production was significantly increased in Dahl S rats on high Na intake, and urinary protein excretion, an index of renal damage, was 273 ± 32 mg/d in S high Na-fed rats and 35 ± 4 mg/d in R high Na-fed rats ( P < 0.05). In conclusion, salt-sensitive hypertension in the S rat is accompanied by marked decreases in renal medullary SOD and greater renal oxidative stress and renal damage than in R rats.

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