Hesperidin ameliorates trichloroethylene-induced nephrotoxicity by abrogation of oxidative stress and apoptosis in wistar rats

Siddiqi, Aisha; Nafees, Sana; Rashid, Summya; Sultana, Sarwat; Saidullah, Bano

doi:10.1007/s11010-015-2400-8

Cited by 26 publications

(15 citation statements)

References 63 publications

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“…44 Previous studies have shown that cisplatin treatment decreases CAT activity in kidney tissue. 45,46 Our results are supported in another study by Siddiqi et al 47 They reported that in trichloroethylene-induced nephrotoxicity, kidney CAT activity was significantly increased by hesperidin administration in Wistar rats. Ma et al 44 suggest that CAT and its derivatives inhibit cisplatin-induced nephrotoxicity.…”

Section: 6supporting

confidence: 83%

Potential of morin and hesperidin in the prevention of cisplatin-induced nephrotoxicity

Kaltalıoğlu

Cevher

2016

Renal Failure

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Oxidative stress is one of the important mechanisms of cisplatin-induced nephrotoxicity. Therefore, this study was designed to explore the potential protective effects of morin and/or hesperidin on oxidative stress in cisplatin-induced nephrotoxicity. This study was performed on 42 Wistar rats. Rats were divided into seven groups: control, morin, hesperidin, cisplatin, cisplatin þ morin, cisplatin þ hesperidin, and cisplatin þ morin þ hesperidin. Morin and/or hesperidin were given for 10 consecutive days by oral gavage and on the 4th day a single dose of cisplatin (7 mg/kg) was injected intraperitoneally. After administrations, on the 11th day of the experiment the animals were killed, and malondialdehyde (MDA), nitric oxide (NOx), glutathione (GSH) levels and myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD) activity were measured. Cisplatin-treated rats showed increased levels of MDA, and decreased levels of NOx also activity of CAT. Morin and/or hesperidin pretreatment prevent oxidative stress in kidney tissue, while they increase the NOx level, CAT activity, and decrease MPO activity. In conclusion, morin þ hesperidin pretreatment may have a significant potential for protection of cisplatin-induced nephrotoxicity.ARTICLE HISTORY

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Section: 6supporting

confidence: 83%

Potential of morin and hesperidin in the prevention of cisplatin-induced nephrotoxicity

Kaltalıoğlu

Cevher

2016

Renal Failure

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“…By contrast, it can accelerate cell apoptosis (13). Siddiqi et al suggested that hesperidin ameliorates trichloroethylene-induced nephrotoxicity through altering the expression of caspase-3, bax and bcl-2 in Wistar rats (29). The present study indicated that hesperidin significantly prevented the activities of caspase-3 Figure 10.…”

Section: Discussionsupporting

confidence: 46%

Preventive effect of hesperidin modulates inflammatory responses and antioxidant status following acute myocardial infarction through the expression of PPAR‑γ and Bcl‑2 in model mice

Meng

Guo

et al. 2017

Mol Med Report

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Hesperetin is the main pharmacological ingredient of fruit of the citrus family, rutaceae. It is a flavanone, which has potent antioxidation and anti‑inflammatory activities. The present study investigated the preventive effect of hesperidin in the modulation of acute myocardial infarction (AMI)‑induced inflammatory responses and antioxidant status in a mouse model. The levels of creatine kinase‑MB, tumor necrosis factor (TNF‑α), interleukin (IL)‑1β, IL‑6, monocyte chemoattractant protein 1 (MCP‑1), intercellular adhesion molecule 1 (ICAM‑1), malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and caspase‑3/9 were measured using ELISA kits. Western blot analysis analyzed p53 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2, and induced the expression of peroxisome proliferator‑activated receptor‑γ (PPAR‑γ). Hesperidin markedly decreased the myocardial infarction area, heart weight/body weight ratio and activity of creatine kinase‑MB in AMI mice. Hesperidin treatment caused a significant decrease in the levels of TNF‑α, IL‑1β, IL‑6, MCP‑1, ICAM‑1, MDA, CAT, SOD and caspase‑3/9 in mice with AMI. Hesperidin also significantly suppressed the protein expression levels of p53 and Bax/Bcl‑2, and induced the expression of peroxisome proliferator‑activated receptor‑γ (PPAR‑γ) in mice with AMI. The preventive effect of hesperidin modulated the inflammatory response and antioxidant status following AMI through downregulation of the expression of PPAR‑γ and Bcl‑2 in the model mice.

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“…Siddiqi et al reported that pretreatment with hesperidin as an antioxidant agent considerably reduced lipid peroxidation, elevation of oxidative enzymes level, blood urea and Cr concentrations in rats exposed to TCE. These results indicate that hesperidin can function as a protective agent against TCE caused nephrotoxicity ( 12 ).…”

Section: Introductionmentioning

confidence: 91%

“…Increasing evidences indicated that TCE induced oxidative stress to rat kidney tissue and alter their metabolic functions ( 5 , 8 , 10 - 14 ). Numerous studies have shown that antioxidant agents can protect kidney against TCE-induced toxicity ( 10 , 12 - 14 ). Siddiqi et al reported that pretreatment with hesperidin as an antioxidant agent considerably reduced lipid peroxidation, elevation of oxidative enzymes level, blood urea and Cr concentrations in rats exposed to TCE.…”

Section: Introductionmentioning

confidence: 99%

Ameliorative effect of vitamin E on trichloroethylene-induced nephrotoxicity in rats

Heydari¹,

Ahmadizadeh²,

Angali³

2016

J Nephropathol

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Background: 1,1,2-Trichloroethylene (TCE) is an important organic solvent which is widespread in the environment. Work place exposure to TCE has been associated adverse effects in many organs including kidney. Vitamin E is an antioxidant that can overcome oxidative stress. Objectives: The aim of the present study is to examine the role of vitamin E against destructive effects of TCE on rat kidney. Materials and Methods: A total of 35 male Wistar rats were randomly divided into seven groups of equal number in each. The rats in group I were the controls received vehicle only. Animals in groups III, V and VII received intraperitoneal injection (i.p) of corn oil. Rats in groups of II, IV, and VI were received vitamin E at a dose of 200 mg/kg; 30 minutes later, animals were received TCE (i.p) at doses of 1000 mg/kg (groups II and III), 1500 mg/kg (groups of IV and V), and 2000 mg/kg (groups of VI and VII) respectively. The experiment repeated for 7 consecutive days. Twenty-four hours after last administration, animals were killed with overdose of sodium pentobarbital. Blood samples were analyzed for blood urea nitrogen (BUN) and creatinine (Cr). One part of the kidney tissues were excised for measuring malondialdehyde (MDA) and glutathione (GSH) concentrations. Another part were excised for histopathological estimation. Results: TCE induced a dose-dependent elevation in BUN, Cr, MDA and markedly decreased GSH level when compared to those in control rats. TCE-induced dose-dependent injury in rat kidney tissue. Vitamin E significantly decreased BUN, Cr, MDA and increased GSH levels and protected kidney damage in TCE treated animals. Conclusions: The observations suggest that vitamin E may have a protective effect against TCE-induced oxidative stress in the rat kidney.

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Hesperidin ameliorates trichloroethylene-induced nephrotoxicity by abrogation of oxidative stress and apoptosis in wistar rats

Cited by 26 publications

References 63 publications

Potential of morin and hesperidin in the prevention of cisplatin-induced nephrotoxicity

Potential of morin and hesperidin in the prevention of cisplatin-induced nephrotoxicity

Preventive effect of hesperidin modulates inflammatory responses and antioxidant status following acute myocardial infarction through the expression of PPAR‑γ and Bcl‑2 in model mice

Ameliorative effect of vitamin E on trichloroethylene-induced nephrotoxicity in rats

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