A molecular mechanism on the antiapoptotic effects of zingerone in isoproterenol induced myocardial infarcted rats

Prince, P. Stanely Mainzen; Hemalatha, K.

doi:10.1016/j.ejphar.2017.09.051

Cited by 20 publications

(10 citation statements)

References 30 publications

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“…In the present work, ISO-treated groups showed a significant increase in the oxidative stress markers (TBARS) with subsequent depletion of endogenous antioxidants (GSH, SOD, CAT, and GPx), which is known as a experimental and clinical marker of tissue damage [43,44]. The appearance of cardiac oxidative stress might be due to free radical production which mediate myocardial membrane dysfunction following isoproterenol intoxication [28]. However, precotreatment with 7-hyd.HC lessened the oxidative stress produced by ISO, which reduced lipid peroxidation, and increased the activities of the studied antioxidant enzymes (SOD, CAT, and GPx), as well as GSH contents.…”

Section: Discussionmentioning

confidence: 52%

“…The protein like Bcl-2 is a key regulatory component which protect cells from apoptosis, while Bax and caspase-3, as proapoptotic genes, promotes cell death [29]. Indeed, oxidative stress activates pathways of apoptosis through upregulating Bax protein and caspase enzyme and downregulating the antiapoptotic Bcl-2 [28]. This hypothesis was strengthened by the present study showing that ISO treatment significantly increased the expression of Bax and caspase-3 genes and reduced the expression of Bcl-2 protein compared to the control group, a phenomenon which could increase apoptosis and result in functional abnormalities of the myocardium.…”

Section: Discussionmentioning

confidence: 99%

“…Antiapoptotic Genes by RT-PCR Analysis. The RT-PCR analysis was performed to validate the differential expression of myocardial genes (caspases-3, B-cell lymphoma 2 (Bcl-2), and B-cell lymphoma-2-associated x (Bax)) as previously described by Prince and Hemalatha [28]. The total RNA sample from the heart tissue of control and experimental rats was extracted by an Easy spin column kit (170-8898, Bio-Rad) according to the manufacturer's protocol.…”

Section: Myocardial Expression Of Proapoptotic Andmentioning

confidence: 99%

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(E)-N′-(1-(7-Hydroxy-2-Oxo-2H-Chromen-3-Yl) Ethylidene) Benzohydrazide, a Novel Synthesized Coumarin, Ameliorates Isoproterenol-Induced Myocardial Infarction in Rats through Attenuating Oxidative Stress, Inflammation, and Apoptosis

Feriani

Khdhiri

Tir

et al. 2020

Oxidative Medicine and Cellular Longevity

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The present study was directed to investigate the effect of precotreatment with (E)-N′-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide (7-hyd.HC), a novel potent synthesized coumarin, on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. The hydrazone compound was characterized by IR, 1D, and 2D NMR analyses. Experimental induction of MI in rats was established by ISO (85 mg/kg/day, s.c) for two consecutive days (6th and 7th days). 7-hyd.HC or sintrom was given for 7 days prior and simultaneous to ISO injection. 7-hyd.HC offered a cardiopreventive effect by preventing heart injury marker leakage (LDH, ALT, AST, CK-MB, and cTn-I) from cardiomyocytes and normalizing cardiac function and ECG pattern, as well as improving lipid profile (TC, TG, LDL-C, and HDL-C), which were altered by ISO administration. Moreover, 7-hyd.HC precotreatment significantly mitigated the oxidative stress biomarkers, as evidenced by the decrease of lipid peroxidation and the increased level of the myocardial GSH level together with the SOD, GSH-Px, and catalase activities. 7-hyd.HC inhibited the cardiac apoptosis by upregulating the expression of Bcl-2 and downregulating the expression of Bax and caspase-3 genes. In addition, 7-hyd.HC reduced the elevated fibrinogen rate and better prevented the myocardial necrosis and improved the interstitial edema and neutrophil infiltration than sintrom. Overall, 7-hyd.HC ameliorated the severity of ISO-induced myocardial infarction through improving the oxidative status, attenuating apoptosis, and reducing fibrinogen production. The 7-hyd.HC actions could be mediated by its antioxidant, antiapoptotic, and anti-inflammatory capacities.

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Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Section: Myocardial Expression Of Proapoptotic Andmentioning

confidence: 99%

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(E)-N′-(1-(7-Hydroxy-2-Oxo-2H-Chromen-3-Yl) Ethylidene) Benzohydrazide, a Novel Synthesized Coumarin, Ameliorates Isoproterenol-Induced Myocardial Infarction in Rats through Attenuating Oxidative Stress, Inflammation, and Apoptosis

Feriani

Khdhiri

Tir

et al. 2020

Oxidative Medicine and Cellular Longevity

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show abstract

“…Furthermore, zingerone has higher antioxidant activity than ascorbic acid and exerts a scavenging effect against peroxynitrite formed from the reaction of superoxide and nitric oxide . Recently, accumulating evidence has suggested that zingerone protects the heart from myocardial infarction injury via its antioxidant and free radical scavenging properties . Another study revealed that pretreatment with zingerone relieves hyperlipidaemia and cardiac hypertrophy in isoproterenol‐induced myocardial infarcted rats .…”

Section: Introductionmentioning

confidence: 99%

Zingerone attenuates aortic banding‐induced cardiac remodelling via activating the eNOS/Nrf2 pathway

Liu

Cai

et al. 2019

J Cellular Molecular Medi

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Cardiac remodelling refers to a series of changes in the size, shape, wall thickness and tissue structure of the ventricle because of myocardial injury or increased pressure load. Studies have shown that cardiac remodelling plays a significant role in the development of heart failure. Zingerone, a monomer component extracted from ginger, has been proven to possess various properties including antioxidant, anti‐inflammatory, anticancer and antidiabetic properties. As oxidative stress and inflammation contribute to acute and chronic myocardial injury, we explored the role of zingerone in cardiac remodelling. Mice were subjected to aortic banding (AB) or sham surgery and then received intragastric administration of zingerone or saline for 25 days. In vitro, neonatal rat cardiomyocytes (NRCMs) were treated with zingerone (50 and 250 μmol/L) when challenged with phenylephrine (PE). We observed that zingerone effectively suppressed cardiac hypertrophy, fibrosis, oxidative stress and inflammation. Mechanistically, Zingerone enhanced the nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2)/antioxidant response element (ARE) activation via increasing the phosphorylation of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production. Additionally, we used Nrf2‐knockout (KO) and eNOS‐KO mice and found that Nrf2 or eNOS deficiency counteracts these cardioprotective effects of zingerone in vivo. Together, we concluded that zingerone may be a potent treatment for cardiac remodelling that suppresses oxidative stress via the eNOS/Nrf2 pathway.

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“…Next, we tested the effects of IGF1-24 on cardiac repair in vivo after cardiac damage. Isoproterenol were used to induce myocardial injury [22,23]. As a first step, 6-7-weeks old female SD rats were randomly divided into three groups.…”

Section: Igf1-24 Repaired Cardiac Injury In Vivo After Cardiac Damagementioning

confidence: 99%

Recombinant Protein IGF1-24 Stimulates Rat Cardiomyocytes Proliferation and Repairs Myocardial Injury

Wang

et al. 2020

Preprint

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Mammal cardiomyocytes lose their ability of regeneration shortly after birth. Reduced cardiomyocytes number caused by myocardial damage is unable to reverse in current clinical therapies. Therefore, it is important and urgent to find new approaches to stimulate cardiomyocytes regeneration. Here we design a recombinant protein IGF1-24 and show that it triggers cardiomyocytes proliferation in rat. 7 days after tail intravenous injection of IGF1-24 ， 6-7-weeks-old healthy rats showed marked improvements in cardiomyocytes proliferation. Next, we injured rats cardiac with isoproterenol and treated them with IGF1-24 injection. We found that it efficiently induced cell proliferation with significant improvements in heart histology. These results show that the recombinant IGF1-24 stimulates cardiomyocytes proliferation and can be used to achieve cardiac repair through stimulating endogenous cardiomyocyte proliferation in rats. The IGF 1-24 could be a prospective medicine to heart repair because it has high efficiency in triggering cell proliferation and it can be easily applied to heart by intravenous injection

show abstract

A molecular mechanism on the antiapoptotic effects of zingerone in isoproterenol induced myocardial infarcted rats

Cited by 20 publications

References 30 publications

(E)-N′-(1-(7-Hydroxy-2-Oxo-2H-Chromen-3-Yl) Ethylidene) Benzohydrazide, a Novel Synthesized Coumarin, Ameliorates Isoproterenol-Induced Myocardial Infarction in Rats through Attenuating Oxidative Stress, Inflammation, and Apoptosis

(E)-N′-(1-(7-Hydroxy-2-Oxo-2H-Chromen-3-Yl) Ethylidene) Benzohydrazide, a Novel Synthesized Coumarin, Ameliorates Isoproterenol-Induced Myocardial Infarction in Rats through Attenuating Oxidative Stress, Inflammation, and Apoptosis

Zingerone attenuates aortic banding‐induced cardiac remodelling via activating the eNOS/Nrf2 pathway

Recombinant Protein IGF1-24 Stimulates Rat Cardiomyocytes Proliferation and Repairs Myocardial Injury

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