The Ameliorative Effects of Caffeic Acid Phenethyl Ester in Cisplatin-Induced Nephrotoxicity: Assessment of the Oxidative Stress an Inflammation

Ceylan, Tayfun; Kaymak, Emin; Akın, Aynur; Yakan, Birkan

doi:10.4067/s0717-95022021000200612

Cited by 5 publications

(1 citation statement)

References 27 publications

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“…CA is found mostly as ester conjugates including chlorogenic acids (esters of CA and quinic acid) and other related compounds (Espíndola et al, 2019). The reported pharmacological activities of CA include immunomodulatory activity (Kilani‐Jaziri et al, 2017), antiviral—including the human immunodeficiency virus—and immunostimulatory activity (Kilani‐Jaziri et al, 2017), cardioprotective activity (Agunloye et al, 2019), antidiabetic activity, antiatherosclerotic activity, antiproliferative activity (Xie et al, 2017), hepatoprotective activity (Akçam et al, 2013; Bispo et al, 2017), anticancer activity (Gu et al, 2016; McGlynn et al, 2015), and antioxidant properties (Agunloye et al, 2019; Ceylan et al, 2021; Stahli et al, 2019). The antioxidant activity of CA is due to the possession of delocalized aromatic rings and free electrons or hydrogen atoms that are easily donated to reactive oxygen species to stabilize them (Espíndola et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Caffeic acid mitigates aflatoxinB1‐mediated toxicity in the male rat reproductive system by modulating inflammatory and apoptotic responses, testicular function, and the redox‐regulatory systems

Owumi

Irozuru

Arunsi

et al. 2022

Journal of Food Biochemistry

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Aflatoxin B1 (AFB1) is a toxic metabolite of public health concern. The present study investigates the protective effects of caffeic acid (CA) against AFB1‐induced oxidative stress, inflammation, and apoptosis in the hypothalamus, epididymis, and testis of male rats. Five experimental rat cohorts (n = 6) were treated per os for 28 consecutive days as follows: Control (Corn oil 2 ml/kg body weight), AFB1 alone (50μg/kg), CA alone (40 mg/kg) and the co‐treated rat cohorts (AFB1: 50μg/kg + CA1: 20 or 40 mg/kg). Following sacrifice, the biomarkers of hypothalamic, epididymal, and testicular toxicities, antioxidant enzyme activities, myeloperoxidase (MPO) activity, as well as levels of nitric oxide (NO), reactive oxygen and nitrogen (RONS) species and lipid peroxidation (LPO) were analysed spectrophotometrically. Besides, the concentration of tumour necrosis factor‐alpha (TNF‐α), Bcl‐2 and Bax proteins were assessed using ELISA. Results showed that the AFB1‐induced decrease in biomarkers of testicular, epididymal and hypothalamic toxicity was significantly (p < .05) alleviated in rats coexposed to CA. Moreover, the reduction of antioxidant status and the increase in RONS and LPO were lessened (p < .05) in rats co‐treated with CA. AFB1 mediated increase in TNF‐α, Bax, NO and MPO activity were reduced (p< .05) in the hypothalamus, epididymis, and testis of rats coexposed to CA. In addition, Bcl‐2 levels were reduced in rats treated with CA dose‐dependently. Light microscopic examination showed that histopathological lesions severity induced by AFB1 were alleviated in rats coexposed to CA. Taken together, the amelioration of AFB1‐induced neuronal and reproductive toxicities by CA involves anti‐inflammatory, antioxidant, antiapoptotic mechanisms in rats. Practical applications The beneficial antioxidant effects of caffeic acid (CA) are attributed to CA delocalized aromatic rings and free electrons, easily donated to stabilize reactive oxygen species. We report in vivo findings on CA and AfB1 mediated oxidative stress and reproductive dysfunction in rats. CA conjugated esters including chlorogenic acids are widely distributed in plants, and they act as a dietary source of natural defense against infections. CA can chelate heavy metals and reduce production of damaging free radicals to cellular macromolecules. Along these lines, CA can stabilize aflatoxin B1‐epoxide as well and avert deleterious conjugates from forming with deoxyribonucleic acids. Hence CA, as a dietary phytochemical can protect against the damaging effects of toxins including aflatoxin B1 that contaminate food. CA dose‐dependently abated oxidative, inflammatory, and apoptotic stimuli, improved functional characteristics of spermatozoa and reproductive hormone levels, and prevented histological alterations in experimental rats’ hypothalamus and reproductive organs brought about by AFB1 toxicity.

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Section: Introductionmentioning

confidence: 99%

Caffeic acid mitigates aflatoxinB1‐mediated toxicity in the male rat reproductive system by modulating inflammatory and apoptotic responses, testicular function, and the redox‐regulatory systems

Owumi

Irozuru

Arunsi

et al. 2022

Journal of Food Biochemistry

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Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats

Ceylan

Akın

Karabulut

et al. 2023

J Biochem & Molecular Tox

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Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti‐inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin–eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas‐3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas‐3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis‐associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.

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Caffeic Acid Phenethyl Ester Suppresses Cytokine- and Chemotherapy-Induced Inflammation in Triple-Negative Breast Cancer via NF-κB Signalling

Fosu,

Quarshie,

Offei

et al. 2024

Natural Product Communications

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Background: Triple-negative breast cancer (TNBC) remains a significant clinical challenge due to its aggressive nature and lack of targeted therapies. In TNBC, inflammation contributes to tumour progression by promoting cell proliferation, survival, and migration. It may be triggered by cytokines such as TNF-α or chemotherapeutic agents such as doxorubicin (DOX). Thus, identifying agents that suppress inflammation in TNBC is of prime interest. Caffeic acid phenethyl ester (CAPE) is a naturally occurring anti-inflammatory compound that exhibits selective cytotoxicity against some cancer cells. However, its impact on cytokine or chemotherapy induced inflammation in TNBC has not yet been explored. Aim: This study aimed to investigate the effects of CAPE on TNF-α- or DOX-induced inflammation and metastatic markers in TNBC. Methods: The effects of CAPE and DOX on TNBC cell viability and migration were assessed using the MTT and wound healing assays, respectively. The effect of CAPE on the expression of pro-inflammatory cytokines, epithelial-mesenchymal transition (EMT) markers, and tumour invasion markers was evaluated using RT-qPCR. Results: CAPE inhibited TNF-α-induced proliferation and migration of TNBC cells. CAPE also suppressed TNF-α- and DOX-induced upregulation of NF-κB-regulated pro-inflammatory genes, IL-1B, IL-6, IL-8, and TNF-α, corroborating the evidence that CAPE suppresses NF-κB signalling. Additionally, CAPE suppressed EMT in TNF-α–stimulated and DOX-treated cells by downregulating vimentin and VCAM1. Furthermore, CAPE reduced the expression of the cancer invasion markers MMP2 and MMP9. Conclusions: We demonstrated the anticancer potential of CAPE and its ability to suppress cytokine and chemotherapy-induced inflammation. This study offers novel insights into the role of CAPE in suppressing inflammation and metastasis markers in TNBC, specifically in the context of TNF-α and DOX-induced NF-κB signalling. These findings underscore the urgent need to further study CAPE as a possible adjuvant for treating patients with TNBC, especially those undergoing chemotherapy.

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The Ameliorative Effects of Caffeic Acid Phenethyl Ester in Cisplatin-Induced Nephrotoxicity: Assessment of the Oxidative Stress an Inflammation

Cited by 5 publications

References 27 publications

Caffeic acid mitigates aflatoxinB1‐mediated toxicity in the male rat reproductive system by modulating inflammatory and apoptotic responses, testicular function, and the redox‐regulatory systems

Caffeic acid mitigates aflatoxinB1‐mediated toxicity in the male rat reproductive system by modulating inflammatory and apoptotic responses, testicular function, and the redox‐regulatory systems

Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats

Caffeic Acid Phenethyl Ester Suppresses Cytokine- and Chemotherapy-Induced Inflammation in Triple-Negative Breast Cancer via NF-κB Signalling

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