Sinapic Acid Attenuated Cisplatin-Induced Cardiotoxicity by Inhibiting Oxidative Stress and İnflammation with GPX4-Mediated NF-kB Modulation

Yıldırım, Caner; Cangi, Sibel; Örkmez, Mustafa; Yılmaz, Şenay; Bozdayı, Mehmet Akif; Yamaner, Hatice; Cevik, Sena

doi:10.1007/s12012-022-09773-3

Cited by 10 publications

(5 citation statements)

References 48 publications

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“…As Figure 7(E) shown that after free DOX treated, myocardial tissue showed strong fibrosis (blue area) (Yildirim et al., 2023 ). At the same time, no obvious fibrosis was observed in PEI-DOX/EGCG and PEI-DOX/EGCG/FA group, which indicating that EGCG could remove oxygen free radicals in the body and reducing the cardiotoxicity of DOX in a further step.…”

Section: Resultsmentioning

confidence: 88%

Enhanced therapeutic efficacy of doxorubicin against multidrug-resistant breast cancer with reduced cardiotoxicity

Zhang

Wang

et al. 2023

Drug Delivery

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Doxorubicin (DOX), a commonly used anti-cancer drug, is limited by its cardiotoxicity and multidrug resistance (MDR) of tumor cells. Epigallocatechin gallate (EGCG), a natural antioxidant component, can effectively reduce the cardiotoxicity of DOX. Meanwhile, EGCG can inhibit the expression of P-glycoprotein (P-gp) and reverse the MDR of tumor cells. In this study, DOX is connected with low molecular weight polyethyleneimine (PEI) via hydrazone bond to get the pH-sensitive PEI-DOX, which is then combined with EGCG to prevent the cardiotoxicity of DOX and reverse the MDR of cancer cells. In addition, folic acid (FA) modified polyethylene glycol (PEG) (PEG-FA) is added to get the targeted system PEI-DOX/EGCG/FA. The MDR reversal and targeting ability of PEI-DOX/EGCG/FA is performed by cytotoxicity and in vivo anti-tumor activity on multidrug resistant MCF-7 cells (MCF-7/ADR). Additionally, we investigate the anti-drug resistant mechanism by Western Blot. The ability of EGCG to reduce DOX cardiotoxicity is confirmed by cardiotoxicity assay. In conclusion, PEI-DOX/EGCG/FA can inhibit the expression of P-gp and reverse the MDR in tumor cells. It also shows the ability of remove oxygen free radicals effectively to prevent the cardiotoxicity of DOX.

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Section: Resultsmentioning

confidence: 88%

Enhanced therapeutic efficacy of doxorubicin against multidrug-resistant breast cancer with reduced cardiotoxicity

Zhang

Wang

et al. 2023

Drug Delivery

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“…Similarly, in RAW264.7 macrophages, the anti-inflammatory effects of SA were found to be due to the suppression of COX-2, TNF-α, and IL-1β expression . Multiple studies have linked SA’s anti-inflammatory effect to NF-κB modulation and the expression of pro-inflammatory cytokines, which play a crucial role in safeguarding the mouse liver against inflammation induced by carbon tetrachloride. ,, …”

Section: Propertiesmentioning

confidence: 99%

“…24 Multiple studies have linked SA's anti-inflammatory effect to NF-κB modulation and the expression of proinflammatory cytokines, which play a crucial role in safeguarding the mouse liver against inflammation induced by carbon tetrachloride. 13,57,58 7.3. Antiapoptotic.…”

Section: Toxicitymentioning

confidence: 99%

Pharmacological Activities and Molecular Mechanisms of Sinapic Acid in Neurological Disorders

Farzan,

Abedi,

Bhia

et al. 2024

ACS Chem. Neurosci.

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Sinapic acid (SA) is a phenylpropanoid derivative found in various natural sources that exhibits remarkable versatile properties, including antioxidant, anti-inflammatory, and metalchelating capabilities, establishing itself as a promising candidate for the prevention and treatment of conditions affecting the central nervous system, such as Alzheimer's disease (AD), Parkinson's disease (PD), ischemic stroke, and other neurological disorders. These effects also include neuroprotection in epilepsy models, as evidenced by a reduction in seizure-like behavior, cell death in specific hippocampal regions, and lowered neuroinflammatory markers. In AD, SA treatment enhances memory, reverses cognitive deficits, and attenuates astrocyte activation. SA also has positive effects on cognition by improving memory and lowering oxidative stress. This is shown by lower levels of oxidative stress markers, higher levels of antioxidant enzyme activity, and better memory retention. Additionally, in ischemic stroke and PD models, SA provides microglial protection and exerts anti-inflammatory effects. This review emphasizes SA's multifaceted neuroprotective properties and its potential role in the prevention and treatment of various brain disorders. Despite the need for further research to fully understand its mechanisms of action and clinical applicability, SA stands out as a valuable bioactive compound in the ongoing quest to combat neurodegenerative diseases and enhance the quality of life for affected individuals.

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“…); electrocardiography anomalies; thromboembolic; cardiomyopathy; and congestive heart failure [22,30]. The excess in producing high levels of oxidative stress also underlines the arising of cisplatin toxicity in the cardiovascular system [37,38].…”

Section: Role Of Cisplatin-induced Oxidative Stress In Tissue Injurymentioning

confidence: 99%

“…Mainly rats are used as an animal model for the purposes of such in vivo experiments. Thus, recent studies, such as the one reported by Yildirim et al [38], used Sprague-Dawley rats (8-10 weeks old) for evaluating the effects of sinapic acid on cisplatin-induced toxicity. Sinapic acid (20 mg/kg/day) was administered to rats intragastrically for five weeks, while a single dose of cisplatin (3 mg/kg, i.p.)…”

Section: Overview Of Recent Relevant Animal Modelsmentioning

confidence: 99%

Oxidative Damage as a Fundament of Systemic Toxicities Induced by Cisplatin—The Crucial Limitation or Potential Therapeutic Target?

Katanić Stanković,

Selaković,

Rosić

2023

IJMS

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Cisplatin, an inorganic complex of platinum, is a chemotherapeutic drug that has been used for 45 years. Despite the progress of pharmaceutical sciences and medicine and the successful application of other platinum complexes for the same purpose, cisplatin is still the therapy of choice in many cancers. Treatment for testicular, ovarian, head and neck, urothelial, cervical, esophageal, breast, and pulmonary malignancies is still unthinkable without the use of this drug. However, cisplatin is also known for many side effects, of which the most pronounced are nephrotoxicity leading to acute renal failure, neurotoxicity, and ototoxicity. Mechanistic studies have proven that one of the conditions that plays a major role in the development of cisplatin-induced toxicities is oxidative stress. Knowing the fact that numerous antioxidants can be used to reduce oxidative stress, thereby reducing tissue lesions, organ failure, and apoptosis at the cellular level, many studies have defined antioxidants as a priority for investigation as a cotreatment. To investigate the mechanism of antioxidant action in vivo, many animal models have been employed. In the last few years, studies have mostly used rodents and zebrafish models. In this article, some of the most recent investigations that used animal models are listed, and the advantages and disadvantages of such experimental studies are pointed out.

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Sinapic Acid Attenuated Cisplatin-Induced Cardiotoxicity by Inhibiting Oxidative Stress and İnflammation with GPX4-Mediated NF-kB Modulation

Cited by 10 publications

References 48 publications

Enhanced therapeutic efficacy of doxorubicin against multidrug-resistant breast cancer with reduced cardiotoxicity

Enhanced therapeutic efficacy of doxorubicin against multidrug-resistant breast cancer with reduced cardiotoxicity

Pharmacological Activities and Molecular Mechanisms of Sinapic Acid in Neurological Disorders

Oxidative Damage as a Fundament of Systemic Toxicities Induced by Cisplatin—The Crucial Limitation or Potential Therapeutic Target?

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