Lutein mitigates cyclophosphamide induced lung and liver injury via NF-κB/MAPK dependent mechanism

El-Kholy, Amal A.; Elkablawy, Mohamed A.; El‐Agamy, Dina S.

doi:10.1016/j.biopha.2017.05.103

Cited by 48 publications

(35 citation statements)

References 43 publications

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“…In CP-induced hepatotoxicity, cellular damage led to the increased cytosolic enzymes levels (AST, ALT, and LDH) in the blood( 31 ). In this study, a rise in the hepatic index such as ALT, AST, and LDH in serum were observed in CP-induced heptatotoxicy, that were consistent with previous studies( 32 ). Antioxidants are effective in the protection of hepatotoxicity undergoing chemotherapy( 4 ).…”

Section: Discussionsupporting

confidence: 93%

Atorvastatin mitigates cyclophosphamide-induced hepatotoxicity via suppression of oxidative stress and apoptosis in rat model

et al. 2018

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Cyclophosphamide (CP), as a chemotherapy drug, induces hepatotoxicity through causing oxidative stress. Atorvastatin (ATV) at a low dose has antioxidant and anti-inflammatory properties. The present study was designed to investigate the protective effects of ATV against CP-induced hepatotoxicity in rat. In this experimental study, 32 rats were treated with ATV orally at a dose of 10 mg/kg for 10 consecutive days, 5 days before and 5 days after the administration of a single intraperitoneal injection of CP (150 mg/kg). The hepatoprotective effect of ATV was evaluated by measuring liver function markers, oxidative markers, histological and immunohistochemical assays. The biochemical results showed that administration of CP increased hepatic biomarkers enzymes as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels. CP increased malondialdehyde (MDA), protein carbonyl (PC) and decreased glutathione (GSH) content in rats. Moreover, administration of CP was associated with periportal leucocyte infiltration, dilation sinusoids, hepatocyte vacuolation, congestion and hemorrhage in livers of rats. CP significantly increased immunoreactivity of caspase-3 as a marker of apoptosis in liver tissue. ATV markedly mitigated liver injury through reduction in oxidative stress biomarkers, histopathological findings and apoptosis. The antioxidant and anti-apoptotic activities of ATV are main proposed mechanisms involved in its hepatoprotective effects against CP-induced hepatic injury.

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Section: Discussionsupporting

confidence: 93%

Atorvastatin mitigates cyclophosphamide-induced hepatotoxicity via suppression of oxidative stress and apoptosis in rat model

et al. 2018

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“…Cyclophosphamide activates the p38 mitogen-activated protein kinase (p38-MAPK) pathway, and it can induce an oxidative injury [50]. Cyclophosphamide-enhanced proinflammatory/proapoptotic activities are reported to result in cardiomyopathy, myocardial infarction, and heart failure [13].…”

Section: Pathophysiology Of Cyclophosphamide-induced Cardiotoxicitymentioning

confidence: 99%

The Role of Antioxidants in Ameliorating Cyclophosphamide-Induced Cardiotoxicity

Ayza

Zewdie

Tesfaye

et al. 2020

Oxidative Medicine and Cellular Longevity

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The chemotherapeutic and immunosuppressive agent cyclophosphamide has previously been shown to induce complications within the setting of bone marrow transplantation. More recently, cardiotoxicity has been shown to be a dose-limiting factor during cyclophosphamide therapy, and cardiooncology is getting wider attention. Though mechanism of cyclophosphamide-induced cardiotoxicity is not completely understood, it is thought to encompass oxidative and nitrative stress. As such, this review focuses on antioxidants and their role in preventing or ameliorating cyclophosphamide-induced cardiotoxicity. It will give special emphasis to the cardioprotective effects of natural, plant-derived antioxidants that have garnered significant interest in recent times.

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“…In recent years, abundant reports have showed that MAPKs signal pathway played an essential role in the regulation of inflammation responses during liver injury . A recent report showed that the activation of MAPKs in the rat liver was linked with cell death via oxidative stress .…”

Section: Resultsmentioning

confidence: 99%

“…In recent years, abundant reports have showed that MAPKs signal pathway played an essential role in the regulation of inflammation responses during liver injury. [27][28][29] A recent report showed that the activation of MAPKs in the rat liver was linked with cell death via oxidative stress. [30] The active MAPKs signal pathway could induce transcriptional factor activation and then contribute to activation of macrophages, epithelial cells and endothelial cells, production of cytokines and chemokines that in turn trigger cytokine storm and lead to liver injury in vivo.…”

Section: Gme Attenuates Ald Via the Mapk Pathwaymentioning

confidence: 99%

Anti-alcohol liver disease effect of Gentianae macrophyllae extract through MAPK/JNK/p38 pathway

Cui

Jiang

Shao

et al. 2019

Journal of Pharmacy and Pharmacology

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Objectives The hepatoprotective effect of Gentianae macrophyllae root extract (GME) on alcoholic liver disease (ALD) was evaluated through ethanol induced ALD animal model. Methods Mice were randomly divided into control normal group (10 mice), ethanol‐induced ALD model group (10 mice) and GME plus ethanol group (30 mice). Mice in model group were given intragastric administration with 50% (v/v) ethanol aqueous solution (200 μl for each) once daily for 19 days. Mice in control normal group received equal volumes of water. Mice in GME plus ethanol group were given intragastric administration with 50% (v/v) ethanol aqueous solution (200 μl for each) once daily at 10:00 a.m., after 1 h, mice in GME group sequentially were treated with 20, 40 and 100 mg/kg of GME by gastric gavage for 19 days. the average food and water consumed by the mice in every group were recorded every 2 days and body weight of every mouse in every group was measured every 2 days. Key findings Results showed that GME significantly improved alcohol induced liver injury in a dose‐dependent manner. The impaired hepatic tissue structure was repaired and the collagen deposition declined after GME administration. Meanwhile, the level of malonaldehyde (MDA), Aspartate transaminase (AST) and alanine transaminase (ALT) (indicators of liver damage) in blood serum were significantly controlled by GME with a dose‐dependent manner, moreover, body weight and liver index were also improved after administration of GME. Pro‐inflammatory cytokines including MCP‐1, TNF‐α, IL‐1 and IL‐6 were detected through RT‐PCR and ELISA in experiment and GME can significantly inhibit the expression of TNF‐α, IL‐1 and IL‐6 but have no effect on MCP‐1. In order to explore the mechanism of GME on ALD, MAPKs pathway was examined and results indicated that GME attenuated ALD through inhibiting the phosphorylation of JNK and P38 and further suppressing the initiation of inflammation. Conclusions GME attenuated ALD through inhibiting the phosphorylation of JNK and P38 and further suppressing the initiation of inflammation.

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Lutein mitigates cyclophosphamide induced lung and liver injury via NF-κB/MAPK dependent mechanism

Cited by 48 publications

References 43 publications

Atorvastatin mitigates cyclophosphamide-induced hepatotoxicity via suppression of oxidative stress and apoptosis in rat model

Atorvastatin mitigates cyclophosphamide-induced hepatotoxicity via suppression of oxidative stress and apoptosis in rat model

The Role of Antioxidants in Ameliorating Cyclophosphamide-Induced Cardiotoxicity

Anti-alcohol liver disease effect of Gentianae macrophyllae extract through MAPK/JNK/p38 pathway

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