The Effect of Mangiferin Against Brain Damage Caused by Oxidative Stress and Inflammation Induced by Doxorubicin

Siswanto, Soni; Arozal, Wawaimuli; Juniantito, Vetnizah; Grace, Agatha; Agustini, Femmi Dwinda; Nafrialdi, Nafrialdi

doi:10.1016/j.hjb.2016.02.001

Cited by 33 publications

(19 citation statements)

References 33 publications

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“…Tumor necrosis factor -α is a cytokine that has a role in immune response as a reaction to several stresses. Also, it is the cause of cognitive damage in neurodegenerative diseases and stimulates the inflammatory response, which causes many of the clinical problems [9]. The present study found an increase in the TNFα level in the brain tissue of DOX-treated group compared to the control group.…”

Section: Discussionsupporting

confidence: 54%

“…Moreover, increasing the TNF-α level played a role in chronic inflammation, which leads to neuronal death and neurodegenerative diseases. Therefore, the elevation in TNF-α level may be the linkage between DOX-induced oxidative stress and central nervous system damage [9].…”

Section: Discussionmentioning

confidence: 99%

“…TNF-α migrates across the BBB and activates glial cells to release large amounts of the local TNF-α in the cortex and hippocampus leading to inflammation and induced oxidative stress in the brain [8]. Thus, the increase in TNF-α level may be a reason for doxorubicininduced oxidative stress and its central nervous system injury [9]. Antagonizing circulating TNF-α with TNF-α antibody led to a manifest decrease in TNF-α levels and the observed mitochondrial dysfunction in brain tissues [5].…”

Section: Introductionmentioning

confidence: 99%

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Prophylactic and Ameliorative Effect of N-Acetylcysteine on Doxorubicin-Induced Neurotoxicity in Wister Rats

Mohammed

Radwan

Elsayed

2019

Egyptian Journal of Basic and Clinical Pharmacology

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Doxorubicin (DOX) is an anthracycline antibiotic and a quinone-containing chemotherapeutic drug used for various types of cancers. However, as with most anticancer drugs, it causes many toxic effects, one of them is cognitive impairment. The present study investigated the prophylactic and ameliorative effect of n-acetylcysteine (NAC) against DOX-induced neurotoxicity in rats. Rats were divided into four groups. Control group: rats received saline. NAC treated group: rats received NAC (100 mg/kg, p.o.) daily for 35 days. DOX-treated group: rats received DOX (4 mg/kg, i.p.) for four weeks on day 7, 14, 21 and 28. DOX+NAC treated group 1: rats received NAC (100 mg/kg, p.o.) daily for 35 days and DOX (4 mg/kg, i.p.) for four weeks on day 7, 14, 21 and 28). DOX+NAC treated group 2: rats received NAC (100 mg/kg, p.o.) daily started at the 7th day of the experiment till the end of the experiment and DOX (4 mg/kg, i.p.) for four weeks on day 7, 14, 21 and 28. The present results showed a significant reduction in the body weight, which was associated with a significant increase in brain to body weight ratio in DOX-treated rats. Tumor necrosis factor (TNF-α) level, malondialdehyde (MDA) and total protein levels were significantly elevated. Whilst, reduced glutathione (GSH) and glutathione peroxidase (GPx) levels were significantly decreased. Moreover, there were histopathological abnormalities in the brain tissue of DOX-treated rats, as most of the neurons degenerated and the blood vessels surrounded with wide perivascular spaces. In addition, the neuropil was vacuolated. The present study demonstrated that NAC has a neuroprotective effect on the brain damage induced by DOX, through inhibition of inflammation and oxidative stress. This neuroprotective effect was more pronounced in DOX+NAC treated group 1, as it produced a significant increase in brain GSH and GPx levels and more improvement in the histopathological abnormality compared to DOX+NAC treated group 2.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prophylactic and Ameliorative Effect of N-Acetylcysteine on Doxorubicin-Induced Neurotoxicity in Wister Rats

Mohammed

Radwan

Elsayed

2019

Egyptian Journal of Basic and Clinical Pharmacology

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“…Systemic intraperitoneal administration of DXR, in particular, causes oxidative stress and elevated levels of multidrug resistance-associated protein 1 (MRP1) in the brain (41). Inflammatory markers are detected in both the brain and heart in rats after systemic DXR treatment (42). Though the precise mechanism is still unclear, dysregulated immune response has long been recognized as a feature of autism (43).…”

Section: Discussionmentioning

confidence: 99%

Brain Development and Heart Function after Systemic Single-Agent Chemotherapy in a Mouse Model of Childhood Leukemia Treatment

Noakes

Przybycien

Forwell

et al. 2018

Clinical Cancer Research

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“…Production of reactive oxygen species (ROS) by inhibiting redox cycling and topoisomerase II, mitochondrial dysfunction, apoptosis and dysregulation of autophagy are involved [5][6][7]. In addition to cardiotoxicity, doxorubicin can cause damage in many tissues including liver [8,9], kidney [10], brain [11], lung [12] and testis [13,14].…”

Section: Introductionmentioning

confidence: 99%

Investigation of the Effects of Artemisinin on Testis and Kidney Injury Induced by Doxorubicin

et al. 2019

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Artemisinin, an antimalarial drug, has anticancer activity and possesses protective effects against several tissue injuries. The aim of the present study was to investigate the effects of artemisinin on doxorubicin-induced renal and testicular toxicity in rats. Doxorubicin was administered to rats at a single dose of 10 mg/kg body weight (b.w.) as a single intraperitoneal injection. Application of artemisinin was by using oral gavage feeding needle for 14 days at different specified doses (7 mg/kg and 35 mg/kg b.w.). At the end of the experiments, kidney and testis samples were collected and used for histopathological and immunohistochemical examinations. At histopathological examination, while hyperemia was the marked finding in kidney and testis of rats treated with doxorubicin only, no evidence of structural abnormalities showed in other groups. Immunohistochemical examination of the testes and kidneys demonstrated significantly increased expression of caspase-3, TNF-α, iNOS and NF-κB in rats treated with doxorubicin only. Artemisinin decreased the doxorubicin-induced overexpression of NF-κB, iNOS, TNFα and caspase-3 in these tissues of rats. Artemisinin can protect the kidney and testis against doxorubicin-induced nephrotoxicity and testotoxicity, probably through a decrease of caspase-3, TNF-α, iNOS and NF-κB expressions. It may be concluded that artemisinin has a potential for clinical use in the treatment of kidney and testis damage induced by doxorubicin. Further researches are required to determine the appropriate combination of artemisinin with doxorubicin.

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The Effect of Mangiferin Against Brain Damage Caused by Oxidative Stress and Inflammation Induced by Doxorubicin

Cited by 33 publications

References 33 publications

Prophylactic and Ameliorative Effect of N-Acetylcysteine on Doxorubicin-Induced Neurotoxicity in Wister Rats

Prophylactic and Ameliorative Effect of N-Acetylcysteine on Doxorubicin-Induced Neurotoxicity in Wister Rats

Brain Development and Heart Function after Systemic Single-Agent Chemotherapy in a Mouse Model of Childhood Leukemia Treatment

Investigation of the Effects of Artemisinin on Testis and Kidney Injury Induced by Doxorubicin

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