The perfusion of cisplatin and cisplatin structural analogues through the isolated rat heart: The effects on coronary flow and cardiodynamic parameters

Milosavljevic, Isidora; Jakovljević, Vladimir; Živković, Vladimir; Srejović, Ivan; Nikolić, Tamara; Jeremić, Jovana; Jeremić, Nevena; Djuric, Dragan; Radonjić, Katarina; Labudović‐Borović, Milica; Bugarčić, Živadin D.; Bogojeski, Jovana; Novokmet, Slobodan

doi:10.4149/gpb_2018004

Cited by 7 publications

(2 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, cisplatin is associated with a number of adverse effects including nephrotoxicity 2 , neurotoxicity 3 and ototoxicity 4 . Cardiac injury is one of the important side effects of cisplatin 5 , 6 , and it may severely hamper the use of cisplatin in cancer patients. Therefore, there is a need to identify new targets or new therapeutic interventions to prevent or attenuate deleterious effects of cisplatin on the heart.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of melatonin in cisplatin-induced cardiac toxicity: possible role of BDNF-TNF-α signaling pathway

Zhuo¹,

Jiang²

2022

Acta Cir. Bras.

View full text Add to dashboard Cite

Purpose: The present study explored the role of melatonin in cisplatin-induced cardiac injury along with the possible role of brain-derived neurotrophic factor (BDNF) in melatonin-mediated effects. Methods: Wistar rats were administered cisplatin (10 mg/kg), and cardiac injury was assessed by measuring the levels of cardiac troponin (cTnT) and lactate dehydrogenase (LDH-1).The extent of apoptosis was measured by measuring caspase-3 (pro-apoptotic) and Bcl-2 (anti-apoptotic) in hearts. The levels of BDNF, tumour necrosis factor α (TNF-α) and reduced glutathione were measured in heart. Melatonin (5 and 10 mg/kg) was administered for 15 days, and the role of BDNF was identified by co-administering BDNF inhibitor, ANA-12 (0.25 and 0.5 mg/kg). Results: Melatonin attenuated cTnT and LDH-1 levels along with reduction in caspase-3 and increase in Bcl-2. It also increased cisplatin-induced decrease in BDNF, increase in TNF-α and decrease in reduced glutathione levels. Moreover, ANA-12 abolished the cardioprotective effects, anti-inflammatory and antioxidant effects of melatonin suggesting the role of BDNF in melatonin-mediated effects in cisplatin-induced cardiac injury. Conclusions: Melatonin is useful in cisplatin-induced cardiac injury, which may be due to an increase in BDNF, decrease in inflammation and increase in antioxidant activities.

show abstract

Section: Introductionmentioning

confidence: 99%

Protective effects of melatonin in cisplatin-induced cardiac toxicity: possible role of BDNF-TNF-α signaling pathway

Zhuo¹,

Jiang²

2022

Acta Cir. Bras.

View full text Add to dashboard Cite

show abstract

“…Cisplatin is an inorganic platinum chemotherapy drug that is commonly used in clinical chemotherapy treatment (Yang et al, 2018) because it can effectively treat a wide range of solid tumors, including lung, ovarian, and bladder cancers. However, cisplatin has many serious side effects, such as myelosuppression, nephrotoxicity, and ototoxicity (Stojic et al, 2018), and these toxic side effects limit the clinical application of cisplatin as part of standard cancer treatment. The kidney is considered the main pathway for cisplatin excretion and the main site of its accumulation (Arany and Safirstein, 2003).…”

Section: Introductionmentioning

confidence: 99%

Farrerol Attenuates Cisplatin-Induced Nephrotoxicity by Inhibiting the Reactive Oxygen Species-Mediated Oxidation, Inflammation, and Apoptotic Signaling Pathways

Wei

Fan

et al. 2019

Front. Physiol.

View full text Add to dashboard Cite

Cisplatin is a chemotherapy drug that is often used in clinical practice, but its frequent use often leads to nephrotoxicity. Therefore, we urgently need a drug that reduces the nephrotoxicity induced by cisplatin. Farrerol reportedly has antioxidant potential, but its renal protective effects and potential mechanisms remain unclear. In this study, we used both cell and mouse models to determine the mechanism of farrerol in cisplatin-induced nephrotoxicity. The in vitro experiments revealed that farrerol improved cisplatin-induced nephrotoxicity and reactive oxygen species (ROS) production via nuclear factor erythrocyte 2-related factor 2 (Nrf2) activation. Moreover, farrerol effectively activated Nrf2 and subsequently increased the expression of Nrf2-targeted antioxidant enzymes, including heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase-1 (NQO1), but inhibited Kelch-like ECH-associated protein 1 (Keap1) and NADPH oxidase type 4 (NOX4). Furthermore, farrerol attenuated the phosphorylation of C-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 mitogen-activated protein kinase (p38); the activation of phosphorylated nuclear factor-κB (p-NF-κB) and nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3); and the expression of phosphorylated p53 (p-p53), Bax, and cleaved caspase-3. In vivo, farrerol significantly improved cisplatin-induced renal damage, as demonstrated by the recovery of blood urea nitrogen (BUN), serum creatinine (SCr), kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and pathological damage. Moreover, farrerol inhibited inflammatory and apoptotic protein expression in vivo. Notably, farrerol exerted slight protection in Nrf2-knockout mice compared with wild-type mice. These findings indicate that farrerol can effectively activate Nrf2 and can serve as a therapeutic target in the treatment of acute kidney injury (AKI).

show abstract

Sacubitril/valsartan reverses cardiac structure and function in experimental model of hypertension-induced hypertrophic cardiomyopathy

et al. 2023

View full text Add to dashboard Cite

This study evaluated the effect of sacubtril/valsartan on cardiac remodeling, molecular and cellular adaptations in experimental (rat) model of hypertension-induced hypertrophic cardiomyopathy. Thirty Wistar Kyoto rats; 10 normal (control) and 20 rats with con rmed hypertension-induced hypertrophic cardiomyopathy (HpCM) were used for this study. The HpCM group was further subdivided into untreated, and sacubitril/valsartan treated group. Myocardial structure and function were assessed using echocardiography, Langendorff's isolated heart experiment, blood sampling and qualitative polymerase chain reaction. Left ventricular internal diameter in systole (0.5 vs 0.22 cm, P < 0.01) and diastole (0.82 vs 0.50 cm, P < 0.01) were greater in treated compared to untreated HpCM rats. Interventricular septal wall thickness in end-systole was higher in untreated and treated HpCM rats compared to controls (0.22 vs 0.20 vs 0.16 cm, P < 0.05 respectively). Fractional shortening was lower in treated compared to untreated rats (34% vs 43%, P < 0.01). Systolic and diastolic blood pressures decreased by 58 and 37 mmHg (P < 0.01) respectively in treated compared to untreated rats. Similarly, sacubitril/valsartan treatment reduced oxidative stress and apoptosis (reduced expression of Bax and Cas3 genes) compared to untreated rats.There was a regular histomorphology of cardiomyocytes, interstitium, and blood vessels in treated rats compared to untreated HpCM rats which expressed hypertrophic cardiomyocytes, with polymorphic nuclei, prominent nucleoli and moderately dilated interstitium. In experimental model of hypertensioninduced hypertrophic cardiomyopathy, sacubitril/valsartan treatment led to improved cardiac structure, haemodynamic performance, and reduced oxidative stress and apoptosis. Sacubitril/valsartan thus presents as a potential therapeutic strategy resulted in hypertension-induced hypertrophic cardiomyopathy.

show abstract

The perfusion of cisplatin and cisplatin structural analogues through the isolated rat heart: The effects on coronary flow and cardiodynamic parameters

Cited by 7 publications

References 22 publications

Protective effects of melatonin in cisplatin-induced cardiac toxicity: possible role of BDNF-TNF-α signaling pathway

Protective effects of melatonin in cisplatin-induced cardiac toxicity: possible role of BDNF-TNF-α signaling pathway

Farrerol Attenuates Cisplatin-Induced Nephrotoxicity by Inhibiting the Reactive Oxygen Species-Mediated Oxidation, Inflammation, and Apoptotic Signaling Pathways

Sacubitril/valsartan reverses cardiac structure and function in experimental model of hypertension-induced hypertrophic cardiomyopathy

Contact Info

Product

Resources

About