Relationship between Apoptosis and Expression of Heat Shock Proteins in Peripheral Blood Lymphocytes of Patients with Myocardial Infarction

Константинова, Е. В.; Khomyakova, N. F.; Константинова, Н. А.; Podkolzina, A. V.; Sapozhnikov, Alexander M.

doi:10.1007/s10517-011-1222-2

Cited by 6 publications

(5 citation statements)

References 9 publications

(16 reference statements)

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“…The caspase-3, the reliable marker of apoptosis and the final common product of the extrinsic and intrinsic apoptotic pathways, was significantly increased in the ISP group [ 77 ]. The persistent apoptosis after MI leads to myocardial fibrosis, cardiac remodeling, and pathological alteration in cardiac function [ 78 , 79 ]. The results of our study revealed that pre-and co-treatment with TQ in the third group significantly attenuated apoptosis by decreasing the myocardial tissue level of caspase-3, which indicates the anti-apoptotic properties of TQ.…”

Section: Discussionmentioning

confidence: 99%

Thymoquinone protects against cardiac mitochondrial DNA loss, oxidative stress, inflammation and apoptosis in isoproterenol-induced myocardial infarction in rats

Khalifa

Rashad

El-Hadidy

2021

Heliyon

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Introduction Myocardial infarction (MI) is an ischemic life-threatening disease with exaggerated oxidative stress state that vigorously damages the cardiomyocyte membrane and subcellular structures, including the vital mitochondrial DNA (mtDNA). The mtDNA is responsible for the proper functionality of the mitochondria, which are abundant in cardiomyocytes due to their dynamic nature and energy production requirements. Furthermore, oxidative stress triggers an inflammatory cascade and eventual apoptosis, which exacerbates cardiac injuries and dysfunction. Aim The present study used an isoproterenol (ISP)-induced MI rat model to investigate the role of the main active constituent of Nigella Sativa seeds, thymoquinone (TQ), in preserving the cardiac mtDNA content and ameliorating oxidative stress, inflammation, and apoptosis. Methods Rats in the (TQ + ISP) group were pre-treated with TQ (20 mg/kg/day) for 21 days before the MI induction using ISP (85 mg/kg/day). In addition, negative control and ISP groups were included in the study for comparison. A histopathological examination was performed and serum cardiac parameters (cTnI and LDH) were assessed. In addition, mtDNA content, oxidative stress parameters (MDA, GSH, SOD, GPx, and CAT), inflammatory mediators (IL-6, IL-1β, and TNF-α), and apoptosis markers (BAX, Bcl2, and caspase-3) were detected. Results The results showed that pre- and co-treatment with TQ in the (TQ + ISP) group reversed the histoarchitecture changes, caused a significant decrease in serum cardiac markers, oxidative stress markers, inflammatory cytokines, the apoptosis process, and preserved the cardiac mtDNA content. Conclusion TQ is a cardioprotective agent with an extended effect on preserving the cardiac mtDNA content, in addition to its powerful antioxidant, anti-inflammatory, and anti-apoptotic action.

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Section: Discussionmentioning

confidence: 99%

Thymoquinone protects against cardiac mitochondrial DNA loss, oxidative stress, inflammation and apoptosis in isoproterenol-induced myocardial infarction in rats

Khalifa

Rashad

El-Hadidy

2021

Heliyon

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“…Persistent MI is accompanied with apoptosis and progressive loss of cells with subsequent cardiac remodeling, ventricular dilation, myocardial fibrosis, gradual decrease of cardiac function and heart failure after progression of myocardial infarction ( Konstantinova et al., 2011 ; Rondeau et al., 2011 ). Bcl-2 expression blocks features of apoptosis, like plasma membrane blebbing, DNA cleavage, and nuclear condensation.…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective effect of thymol against adrenaline-induced myocardial injury in rats

El-Marasy

Awdan

Hassan

et al. 2020

Heliyon

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Cardiovascular disease represents a vital global disease burden. This study aims to assess the possible cardioprotective effect of thymol against adrenaline-induced myocardial injury (MI) in rats. Furthermore the effect of thymol on cardiac function biomarkers, electrocardiogram (ECG) alterations, oxidative stress, inflammation, apoptosis and histopathological changes was assessed. MI was induced by adrenaline (2 mg/kg, s.c.) injected as a single dose for 2 consecutive days (24 h apart). Normal and control groups received the vehicle for 21 consecutive days. The other 3 groups were orally administered thymol (15, 30, 60 mg/kg) for 21 consecutive days and on day 22, adrenaline was injected as a single dose for 2 consecutive days. Then ECG examination, biochemical, histopathological, immunohistochemical analyses were carried out. Thymol reversed adrenaline-induced reduction of heart rate, prolongation of RR interval and elevation of ST interval. Thymol pretreatment significantly reduced serum aspartate dehydrogenase (AST), lactate dehydrogenase (LDH), and creatine kinase (CK) levels in MI rats. Oral pretreatment with thymol increased reduced glutathione (GSH), reduced malondialdehyde (MDA), nuclear factor-kappa B (NF-κB), and interleukin-1β (IL-1β) cardiac contents in MI rats. Additionally, thymol administration significantly decreased protein expression of caspase-3, increased Bcl-2 protein expression in cardiac tissue and ameliorated histopathological changes. This study reveals that thymol exerted cardioprotective effect against adrenaline-induced MI in rats evidenced by improving cardiac function, attenuating ECG and histopathological changes which may be partly mediated through its anti-oxidant, anti-inflammatory and anti-apoptotic effect.

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“…Persistent apoptosis leads to the progressive loss of cells, which is known to be an important cause for myocardial fibrosis, ventricular dilation, cardiac remodeling, gradual decrease of cardiac function and heart failure following myocardial infarction (10,11). Therefore, inhibition of apoptosis following myocardial infarction and protecting myocardial cells against loss has become an important focus (12).…”

Section: Discussionmentioning

confidence: 99%

Effects of curcumin on the apoptosis of cardiomyocytes and the expression of NF-κB, PPAR-γ and Bcl-2 in rats with myocardial infarction injury

Yin

et al. 2016

Experimental and Therapeutic Medicine

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Curcumin is a natural polyphenol with powerful antioxidant and anti-inflammatory properties. The present study evaluated the protective effect of curcumin on myocardial injury in rats as well as the mechanisms underlying these effects, and examined the expression of nuclear factor-κB (NF-κB), peroxisome proliferator-activated receptor-γ (PPAR-γ) and B-cell leukemia/lymphoma-2 (Bcl-2) following myocardial infarction. A rat model of myocardial infarction was successfully established. Hematoxylin and eosin staining showed cellular atrophy and hyperchromatic cytoplasm in the myocardial infarction area. The myocardial cells displayed lysis and breakage of cardiac muscle fibers, karyopyknosis and karyorrhexis associated with infiltration of inflammatory cells and proliferation of fibrous tissue. Curcumin treatment at a dosage of 150 mg/kg/body weight resulted in an increase in surviving cells, fewer apoptotic cells, decreased proliferation of fibrous tissue and reduced infiltration of inflammatory cells, though necrosis was still present compared with the rats without curcumin treatment. The immunohistochemical assay demonstrated that curcumin treatment inhibited the expression of NF-κB, but increased the expression of PPAR-γ. The results of the reverse transcription-polymerase chain reaction indicated that curcumin treatment significantly increased the mRNA expression levels of Bcl-2 (P<0.01). Therefore, curcumin antagonizes cardiomyocyte apoptosis and inhibits inflammatory cell infiltration following myocardial infarction, which may be associated with its inhibitory effects on the expression of NF-κB, and activating effects on the expression of PPAR-γ and Bcl-2 in myocardial cells. Curcumin may be useful in clinical practice for saving more living heart muscle in the area of myocardial infarction and improving cardiac function following the elective opening of obstructed coronary arteries.

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Relationship between Apoptosis and Expression of Heat Shock Proteins in Peripheral Blood Lymphocytes of Patients with Myocardial Infarction

Cited by 6 publications

References 9 publications

Thymoquinone protects against cardiac mitochondrial DNA loss, oxidative stress, inflammation and apoptosis in isoproterenol-induced myocardial infarction in rats

Thymoquinone protects against cardiac mitochondrial DNA loss, oxidative stress, inflammation and apoptosis in isoproterenol-induced myocardial infarction in rats

Cardioprotective effect of thymol against adrenaline-induced myocardial injury in rats

Effects of curcumin on the apoptosis of cardiomyocytes and the expression of NF-κB, PPAR-γ and Bcl-2 in rats with myocardial infarction injury

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