N-acetylcysteine reduces oxidative stress, nuclear factor-κB activity and cardiomyocyte apoptosis in heart failure

Wu, Xiaoyan; Luo, Anyu; Zhou, Yirong; Ren, Jing

doi:10.3892/mmr.2014.2292

Cited by 58 publications

(32 citation statements)

References 46 publications

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“…5 D). This beneficial effect of NAC may be achieved by abolishing of cisplatin-induced oxidative damage, due to diminishing nuclear factor (NF)-κB signaling pathway [68] , which has been noted to cause cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

et al. 2015

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The aim of this study was to estimate the protective effect of N-acetyl-l-cysteine (NAC) against cisplatin-induced cardiotoxicity under conditions of ischemic-reperfusion injury.Wistar albino rats were randomly divided into three groups (n = 8): control, cisplatin (5 mg/kg/w, i.p., 5 weeks) and cisplatin + NAC group (cisplatin – 5 mg/kg/w, i.p. and NAC – 500 mg/kg/w, i.p., 5 weeks). Isolated hearts were perfused according to the modified Langendorff technique at constant pressure (70 cmH2O). Following cardiodynamic parameters were measured: maximum rate of left ventricular pressure development, minimum rate of left ventricular pressure development, left ventricular systolic pressure (SLVP), left ventricular diastolic pressure and heart rate. The ischemic vasodilation episodes were induced by the complete interruption of coronary inflow for 30, 60 and 120 s. The samples of the coronary venous effluent (CVE) were continuously collected during the reperfusion period for determination of coronary flow (CF) rate and oxidative stress markers (H2O2, O2−, NO2− and thiobarbituric acid reactive substances – TBARS).Cisplatin reduced CF, heart rate and overflow (total, maximal and duration of overflow) during reperfusion, and increased SLVP (under basal conditions and after global ischemias). Cisplatin increased levels of H2O2 (under basal conditions), O2− and TBARS (under basal conditions and after ischemia), but decreased NO2− levels (during reperfusion) in CVE, and decreased superoxide dismutase and reduced glutathione in serum. NAC attenuated cisplatin-induced changes of cardiodynamic parameters (except CF under basal conditions) and oxidative stress parameters.Those results suggest that NAC, by decreasing oxidative stress, may be useful in cardioprotection during cisplatin therapy.

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Section: Discussionmentioning

confidence: 99%

The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

et al. 2015

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“…Survivin expression in cardiomyocytes were evaluated qualitatively, where cells positive for cytoplasmic staining were considered immunopositive and taken into account 16 . Although cytoplasmic expression of NF-κB/p65 is detected in most normal cells, only distinct brown nuclear immunostaining (brown granules in the nucleus) is considered as activated NF-κB/p65, and quantified as previously described 31 , 32 . The number of survivin or NF-κB/p65 positive cardiomyocytes was expressed as a percentage (%) according to this formula: …”

Section: Methodsmentioning

confidence: 99%

Simvastatin Protects Cardiomyocytes Against Endotoxin-induced Apoptosis and Up-regulates Survivin/NF-κB/p65 Expression

Nežić

Škrbić

Amidžić

et al. 2018

Sci Rep

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This study is aimed to investigate whether simvastatin induces cardiomyocytes survival signaling in endotoxin (lipopolysaccharide, LSP)-induced myocardial injury, and if so, further to determine a role of survivin in simvastatin-anti-apoptotic effect. Wistar rats were pretreated with simvastatin (10–40 mg/kg po) before a single non-lethal dose of LPS. In myocardial tissue, LPS induced structural disorganization of myofibrils with significant inflammatory infiltrate (cardiac damage score, CDS = 3.87 ± 0.51, p < 0.05), whereas simvastatin dose-dependently abolished structural changes induced by LPS (p < 0.01). Simvastatin in 20 mg/kg and 40 mg/kg pretreatment, dose dependently, attenuated myocardial apoptosis determined as apoptotic index (28.8 ± 4.5% and 18.9 ± 3.5, p < 0.05), decreased cleaved caspase-3 expression (32.1 ± 5.8%, p < 0.01), along with significant Bcl-xL expression in the simvastatin groups (p < 0.01). Interestingly, in the simvastatin groups were determined significantly increased expression of survivin (p < 0.01), but in negative correlation with cleaved caspase-3 and apoptotic indices (p < 0.01). Simvastatin has a cardioprotective effects against LPS induced apoptosis. The effect may be mediated by up-regulation of survivin via activation of NF-κB, which leads to reduced activation of caspase-3 and consequent apoptosis of cardiomyocytes in experimental sepsis.

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“…For example, vitamin E could exert a cardioprotective effect but only against chronic cardiotoxicity, not against the development of chronic cardiomyopathy [ 198 ]. Recently, Wu et al were able to reduce apoptosis in cardiomyocytes and also the oxidative stress in a model of heart failure in Japanese white rabbits, using intravenous injections of doxorubicin after being treated with NAC [ 127 ]. In another experimental trial, it was intended to evaluate the influence of vitamin C on the cytotoxicity caused by antineoplastic agents, such as doxorubicin.…”

Section: Antitumor Therapy Oxidative Stress and Interactions Witmentioning

confidence: 99%

Antioxidant Intake and Antitumor Therapy: Toward Nutritional Recommendations for Optimal Results

Mut-Salud

Álvarez

Garrido

et al. 2015

Oxidative Medicine and Cellular Longevity

148

104

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The role of the induction of oxidative stress as the mechanism of action of many antitumor drugs is acquiring an increasing interest. In such cases, the antitumor therapy success may be conditioned by the antioxidants present in our own body, which can be synthesized de novo (endogenous) or incorporated through the diet and nutritional supplements (exogenous). In this paper, we have reviewed different aspects of antioxidants, including their classification, natural sources, importance in diet, consumption of nutritional supplements, and the impact of antioxidants on health. Moreover, we have focused especially on the study of the interaction between antioxidants and antitumor therapy, considering both radiotherapy and chemotherapy. In this regard, we found that the convenience of administration of antioxidants during cancer treatment still remains a very controversial issue. In general terms, antioxidants could promote or suppress the effectiveness of antitumor treatment and even protect healthy tissues against damage induced by oxidative stress. The effects may depend on many factors discussed in the paper. These factors should be taken into consideration in order to achieve precise nutritional recommendations for patients. The evidence at the moment suggests that the supplementation or restriction of exogenous antioxidants during cancer treatment, as appropriate, could contribute to improving its efficiency.

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N-acetylcysteine reduces oxidative stress, nuclear factor-κB activity and cardiomyocyte apoptosis in heart failure

Cited by 58 publications

References 46 publications

The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

Simvastatin Protects Cardiomyocytes Against Endotoxin-induced Apoptosis and Up-regulates Survivin/NF-κB/p65 Expression

Antioxidant Intake and Antitumor Therapy: Toward Nutritional Recommendations for Optimal Results

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