Protective Role of Quercetin on Polychlorinated Biphenyls (Aroclor‐1254) Induced Oxidative Stress and Apoptosis in Liver of Adult Male Rats

Suganya, S.; Selvakumar, Kandaswamy; Giribabu, K.; Elumalai, Perumal; Basha, Fariya Yasmine Afsar; Mohan, Balasakthi Janani Madhan; Arunakaran, J.

doi:10.1002/jbt.21466

Cited by 27 publications

(20 citation statements)

References 27 publications

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“…In our study, CMN and QR pretreatment significantly reversed the LPO and altered antioxidant status. It has been reported that CMN and QR reduced oxidative stress marker LPO by scavenging ROS (Sekaran et al 2012;Singh and Sharma 2011). In our results, CMN and QR could exert a beneficial action against LPO which may act as an added compensation mechanism to maintain cell integrity and protection against free radical damage.…”

Section: Discussionmentioning

confidence: 98%

“…It is largely present in fruits, vegetables, aromatic plants, tea, and red wine (Pandey and Rizvi 2009). The use of both CMN and QR has been reported as a therapeutic agent to mitigate various kinds of toxicity including cardiotoxicity (Matouk et al 2013;Swamy et al 2012), nephrotoxicity (Ciftci et al 2012;Nabavi et al 2012), hepatotoxicity (Waseem and Parvez 2013;Sekaran et al 2012), and neurotoxicity (Haleagrahara et al 2013;Yadav et al 2011). Pretreatment with CMN and QR was found to modulate mitochondrial dysfunction in rodents, and its property as an antioxidant is widely held to be responsible for its protective effects in the mitochondria (Carrasco-Pozo et al 2012;Sood et al 2011).…”

Section: Introductionmentioning

confidence: 97%

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Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Waseem

Parvez

2015

Protoplasma

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Peripheral neurotoxicity is one of the serious dose-limiting side effects of oxaliplatin (Oxa) when used in the treatment of malignant conditions. It is documented that it elicits major side effects specifically neurotoxicity due to oxidative stress forcing the patients to limit its clinical use in long-term treatment. Oxidative stress has been proven to be involved in Oxa-induced toxicity including neurotoxicity. The mitochondria have recently emerged as targets for anticancer drugs in various kinds of toxicity including neurotoxicity that can lead to neoplastic disease. However, there is paucity of literature involving the role of the mitochondria in mediating Oxa-induced neurotoxicity and its underlying mechanism is still debatable. The purpose of this study was to investigate the dose-dependent damage caused by Oxa on isolated brain mitochondria under in vitro conditions. The study was also designed to investigate the neuroprotective effects of nutraceuticals, curcumin (CMN), and quercetin (QR) on Oxa-induced mitochondrial oxidative stress and respiratory chain complexes in the brain of rats. Oxidative stress biomarkers, levels of nonenzymatic antioxidants, activities of enzymatic antioxidants, and mitochondrial complexes were evaluated against the neurotoxicity induced by Oxa. Pretreatment with CMN and QR significantly replenished the mitochondrial lipid peroxidation levels and protein carbonyl content induced by Oxa. CMN and QR ameliorated altered nonenzymatic and enzymatic antioxidants and complex enzymes of mitochondria. We conclude that CMN and QR, by attenuating oxidative stress as evident by mitochondrial dysfunction, hold promise as agents that can potentially reduce Oxa-induced adverse effects in the brain.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 97%

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Waseem

Parvez

2015

Protoplasma

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“…Quercetin widely exists in various fruits, vegetables and traditional Chinese medicine plants; and whose daily intake is about 3‐38 mg/d . To be a therapeutic agent, quercetin is used to alleviate various diseases, including hepatotoxicity, cardiotoxicity, neurotoxicity and nephrotoxicity . The great effects of quercetin are attributed to its antioxidant and anti‐inflammatory capacity .…”

Section: Introductionmentioning

confidence: 99%

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Tian

Lü

Shi

et al. 2020

J Cellular Molecular Medi

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Epidemiological studies have found that diabetes and cognitive dysfunction are closely related. Quercetin has been certified with the effect on improving diabetes mellitus (DM) and cognitive impairment. However, the effect and related mechanism of quercetin on diabetic encephalopathy (DE) are still ambiguous. In this study, we used the db/db mice (diabetic model) to discover whether quercetin could improve DE through the Sirtuin1/NLRP3 (NOD‐, LRR‐ and pyrin domain‐containing 3) pathway. Behavioural results (Morris water maze and new object recognition tests) showed that quercetin (70 mg/kg) improved the learning and memory. Furthermore, quercetin alleviated insulin resistance and the level of fasting blood glucose. Besides, Western blot analysis also showed that quercetin increased the protein expressions of nerve‐ and synapse‐related protein, including postsynapticdensity 93 (PSD93), postsynapticdensity 95 (PSD95), brain‐derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the brain of db/db mice. Quercetin also increased the protein expression of SIRT1 and decreased the expression of NLRP3 inflammation‐related proteins, including NLRP3, the adaptor protein ASC and cleaved Caspase‐1, the pro‐inflammatory cytokines IL‐1β and IL‐18. In conclusion, the present results indicate that the SIRT1/NLRP3 pathway may be a crucial mechanism for the neuroprotective effect of quercetin against DE.

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“…Furthermore, quercetin also posseses antiapoptotic effects (9) . Some studies have evaluated the antiapoptotic effect of quercetin; however, little data is available regarding the antiapoptotic effect of quercetin on retinal I/R injury (10,11) . In the present study, we aimed to evaluate whether quercetin decreases apoptotic cell loss in a rat retinal I/R injury model.…”

Section: Resultados: a Administração De Quercetina Diminuiu O Afinamementioning

confidence: 99%

Quercetin protects the retina by reducing apoptosis due to ischemia-reperfusion injury in a rat model

Arıkan¹,

Erşan²,

Karaca³

et al. 2015

Arquivos Brasileiros De Oftalmologia

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Purpose: This study aimed to investigate the effect of quercetin on apoptotic cell death induced by ischemia-reperfusion (I/R) injury in the rat retina. Methods: Twenty-four rats were divided into four equal groups: control, ischemic, solvent, and quercetin. I/R injury was achieved by elevating the intraocular pressure above the perfusion pressure. Intraperitoneal injections of 20 mg/kg of quercetin and dimethyl sulfoxide (DMSO) were performed in the quercetin and solvent groups, respectively, immediately prior to I/R injury, and the researchers allowed for the retinas to be reperfused. Forty-eight hours after injury, the thicknesses of the retinal ganglion cell layer (RGCL), inner nuclear layer (INL), inner plexiform layer (IPL), outer plexiform layer (OPL), and outer nuclear layer (ONL) were measured in all groups. Moreover, the numbers of terminal deoxynucleotidyl transferase dUTP nick-end-labeled [TUNEL (+)] cells and caspase-3 (+) cells in both INL and ONL were evaluated in all groups. Results: The administration of quercetin was found to reduce the thinning of all retinal layers. The mean thickness of INL in the quercetin and ischemic groups was 21 ± 5.6 µm and 16 ± 6.4 µm, respectively (P<0.05). Similarly, the mean thickness of ONL in the quercetin and ischemic groups was 50 ± 12.8 µm and 40 ± 8.7 µm, respectively (P<0.05). The antiapoptotic effect of quercetin in terms of reducing the numbers of both TUNEL (+) cells and caspase-3 (+) cells was significant in INL. The mean number of TUNEL (+) cells in INL in the ischemic and quercetin groups was 476.8 ± 45.6/mm 2 and 238.72 ± 251/mm², respectively (P<0.005). The mean number of caspase-3 (+) cells in INL of ischemic and quercetin groups was 633.6 ± 38.7/mm 2 and 342.4 ± 36.1/mm 2 , respectively (P<0.001). Conclusion:The use of quercetin may be beneficial in the treatment of retinal I/R injury because of its antiapoptotic effect on the retinal layers, particularly in INL.

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Protective Role of Quercetin on Polychlorinated Biphenyls (Aroclor‐1254) Induced Oxidative Stress and Apoptosis in Liver of Adult Male Rats

Cited by 27 publications

References 27 publications

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Quercetin protects the retina by reducing apoptosis due to ischemia-reperfusion injury in a rat model

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