Protective effect of nebivolol on doxorubicin-induced cardiotoxicity in rats

Mohamed, Enas Ahmed; Kassem, Hussien Heshmat

doi:10.5114/aoms.2018.79008

Cited by 26 publications

(27 citation statements)

References 26 publications

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“…Earlier preclinical studies have proven nebivolol to be beneficial in the reduction of cardiotoxicity. 10,11 However, such a benefit was not observed in this study.…”

Section: Discussioncontrasting

confidence: 74%

Role of nebivolol in anthracycline-induced cardiotoxicity

2019

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Background: Anthracyclines are extensively used in the treatment of breast cancer. However, these therapeutic agents are responsible for chemotherapy-induced cardiotoxicity. Aim of this study was to assess the effect of use of prophylactic nebivolol for the prevention of anthracycline-induced cardiotoxicity in breast cancer patients.Methods: This was a prospective, randomized, single-blind, and placebo-controlled trial involving 80 participants with breast cancer, scheduled to undergo chemotherapy with doxorubicin. Patients were randomly divided into two groups: the nebivolol group (n=40) to receive nebivolol 5 mg daily and the placebo group (n=40) to receive placebo. All patients were evaluated with baseline Electrocardiogram (ECG) and echocardiography prior to treatment, and at the 6-month follow-up. Echocardiography included 2D echocardiography, colour doppler and tissue doppler imaging.Results: The study groups had comparable baseline echocardiographic variables. At the 6-month echocardiographic follow-up, there were no changes of statistical significance in any 2D echocardiographic variables in either group. However, there were minimal reductions of 0.4% in left ventricular ejection fraction in the nebivolol group (62.2±4.4% to 61.9±4.2%, p=0.75) and 1.6% in the placebo group (62.8±3.6% to 61.8±3.2%, p=0.18). Doppler examinations also did not reveal any statistically significant changes in variables such as peak A velocity, peak E velocity, E/A ratio, isovolumic relaxation time, and isovolemic contraction time in either group.Conclusions: Prophylactic use of nebivolol treatment may possess cardioprotective properties against anthracycline-induced cardiotoxicity in breast cancer patients although not statistically significant in this study.

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“…Earlier preclinical studies have proven nebivolol to be beneficial in the reduction of cardiotoxicity. 10,11 However, such a benefit was not observed in this study.…”

Section: Discussioncontrasting

confidence: 74%

Role of nebivolol in anthracycline-induced cardiotoxicity

2019

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“…Inflammatory processes are activated by the migration of leukocytes, inflammatory chemokines and cytokines to the site of tissue injury. 33 TNF-α is activated before leukocytic infiltration occurs especially in the site of local inflammation. 34 Previous studies have demonstrated that oxidative stress aggravates inflammation in I/R injury.…”

Section: Discussionmentioning

confidence: 99%

“…These findings in our study were in agreement with those reported by previous studies; which used NEB and demonstrated its anti-inflammatory effects. 14,33 Previous studies have demonstrated that increased oxidative stress causes an increase in the expression of apoptosis markers in groups with I-induced and I/R induced injury. 34 In our study, we demonstrated the apoptotic damage induced by I and I/R-induced injury in the ovarian cell by using the TUNEL assay.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of nebivolol on ovarian ischemia–reperfusion injury in rat

Çolak

Gürlek

Topçu

et al. 2020

J of Obstet and Gynaecol

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Aim: Ovarian torsion is a common gynecological emergency of reproductive ages, occurring at rates of 2.7-7.4%. This study aimed to evaluate the antioxidant effects of Nebivolol (NEB) and histopathological changes in experimental ischemic (I) and ischemic-reperfusion (I/R) injury in rat ovaries. Methods: Forty-eight adult female rats were randomly separated into six groups as group 1 (control) receiving an oral saline solution for 3 days; group 2 (I) that underwent ischemia for 3 h with the application of atraumatic vascular clips; group 3 (I/R); group 4 (I + NEB) receiving 10 mg/kg NEB by oral gavage 30 min prior to the ischemia induction; group 5 (I/R + NEB) receiving 10 mg/kg NEB, and group 6 (control + NEB) receiving oral 10 mg/kg NEB for 3 days before ischemia induction followed by consequent reperfusion. Ovarian tissue damage was scored by histopathological analysis. Ovarian tissue malondialdehyde (MDA) and glutathione (GSH) levels were measured biochemically. Results: The levels of MDA and tumor necrosis factor-alpha (TNF-α), and TUNEL assay positivity scores increased in the I and I/R groups. GSH levels decreased in all case groups (P < 0.05). The oral administration of NEB (10 mg/kg) to the I-and I/R-groups reduced the levels of MDA and TNF-α and TUNEL assay immunopositivity scores (P < 0.05). GSH levels increased in the treatment groups. Conclusion: The current experimental ovarian torsion study suggests a protective role for NEB against I and I/R injury in rat ovaries. NEB may be a novel agent for decreasing ovarian I/R injury.

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“…Densitometry analysis was performed using the Image J software (NIH Image, Bethesda, USA). GAPDH was used as the control [23].…”

Section: Western Blot Analysismentioning

confidence: 99%

miR-133a-3p promotes apoptosis and induces cell cycle arrest by targeting CREB1 in retinoblastoma

Liu

Wang

et al. 2020

aoms

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Introduction: Retinoblastoma (RB) is a malignant tumor that is derived from photoreceptors. It is common in children under 3 years old with a family genetic predisposition. MicroRNA-133a-3p (miR-133a-3p) is one of the tumor-related miRNAs that interprets a critical function in the genesis and development of various tumors. This study investigated the effects and underlying mechanisms of miR-133a-3p in RB. Material and methods: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis was used to assess the miR-133a-3p expression in RB tissues and a cell model. MTT assay, western blot, flow cytometry and luciferase reporter assay were performed to evaluate the effect of miR-133a-3p on cell viability, apoptosis and the cell cycle. An RB xenograft model was established to assess the in vivo influence of miR-133a-3p on RB growth. Results: MiR-133a-3p level was reduced in RB tissues and the cell model (p < 0.01 or p < 0.001). Addition of miR-133a-3p reduced cell viability, and increased apoptosis and cell cycle arrest (p < 0.001). Additionally, CREB1 was identified to be the target of miR-133a-3p in RB cell lines (p < 0.001). Cell viability reduction, apoptosis and cell cycle arrest increases mediated by miR-133a-3p were attenuated by CREB1 overexpression (p < 0.001). MiR-133a-3p inhibited tumor growth of RB in vivo (p < 0.001). Conclusions: Our results reveal that miR-133a-3p exhibits anti-cancer effects by targeting CREB1 in RB. This study provides a new direction for effective targeted treatment of this disease.

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Protective effect of nebivolol on doxorubicin-induced cardiotoxicity in rats

Cited by 26 publications

References 26 publications

Role of nebivolol in anthracycline-induced cardiotoxicity

Role of nebivolol in anthracycline-induced cardiotoxicity

Protective effects of nebivolol on ovarian ischemia–reperfusion injury in rat

miR-133a-3p promotes apoptosis and induces cell cycle arrest by targeting CREB1 in retinoblastoma

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