Carnosic acid promotes myocardial antioxidant response and prevents isoproterenol-induced myocardial oxidative stress and apoptosis in mice

Sahu, Bidya Dhar; Putcha, Uday Kumar; Kuncha, Madhusudana; Rachamalla, Shyam Sunder; Sistla, Ramakrishna

doi:10.1007/s11010-014-2092-5

Cited by 43 publications

(43 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rosemary can mimic SOD by removing superoxide radicals[58], which could also explain the lower enzyme activity in cardiac tissue of the supplemented groups. No effect of rosemary was observed on Nrf-2 and HO-1 expression, different from what we expected and from previous reports showing Nrf2 activation after treatment with rosemary compounds[59, 60]. One possible explanation is that in some pathological situations, as in hypoxia, Nrf-2 does not increase.…”

Section: Discussioncontrasting

confidence: 99%

Rosemary supplementation (Rosmarinus oficinallis L.) attenuates cardiac remodeling after myocardial infarction in rats

et al. 2017

View full text Add to dashboard Cite

BackgroundMyocardial infarction (MI) is one of the leading causes of morbidity and mortality worldwide. Dietary intervention on adverse cardiac remodeling after MI has significant clinical relevance. Rosemary leaves are a natural product with antioxidant/anti-inflammatory properties, but its effect on morphology and ventricular function after MI is unknown.Methods and resultsTo determine the effect of the dietary supplementation of rosemary leaves on cardiac remodeling after MI, male Wistar rats were divided into 6 groups after sham procedure or experimental induced MI: 1) Sham group fed standard chow (SR0, n = 23); 2) Sham group fed standard chow supplemented with 0.02% rosemary (R002) (SR002, n = 23); 3) Sham group fed standard chow supplemented with 0.2% rosemary (R02) (SR02, n = 22); 4) group submitted to MI and fed standard chow (IR0, n = 13); 5) group submitted to MI and fed standard chow supplemented with R002 (IR002, n = 8); and 6) group submitted to MI and fed standard chow supplemented with R02 (IR02, n = 9). After 3 months of the treatment, systolic pressure evaluation, echocardiography and euthanasia were performed. Left ventricular samples were evaluated for: fibrosis, cytokine levels, apoptosis, energy metabolism enzymes, and oxidative stress. Rosemary dietary supplementation attenuated cardiac remodeling by improving energy metabolism and decreasing oxidative stress. Rosemary supplementation of 0.02% improved diastolic function and reduced hypertrophy after MI. Regarding rosemary dose, 0.02% and 0.2% for rats are equivalent to 11 mg and 110 mg for humans, respectively.ConclusionOur findings support further investigations of the rosemary use as adjuvant therapy in adverse cardiac remodeling.

show abstract

Section: Discussioncontrasting

confidence: 99%

Rosemary supplementation (Rosmarinus oficinallis L.) attenuates cardiac remodeling after myocardial infarction in rats

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Previous investigation has revealed carnosic acid may attenuate the isoproterenol-induced myocardial injury in a mouse model through preventing oxidative stress and apoptosis (17). In the present study, the investigations performed further elucidated the protective effects of carnosic acid on myocardial injury in vitro, which is reported in H9c2 cardiomyocytes for the first time.…”

Section: Discussionsupporting

confidence: 62%

“…Previous pharmacological studies have demonstrated that carnosic acid affords various biological activities, such as neuroprotection (11), prevention of advanced glycation end-product formation (12), attenuation of Alzheimer's disease (13), anticancer activity (14), anti-inflammation (15) and renoprotection (16). Furthermore, carnosic acid presented a cardioprotective effect in an isoproterenol-induced myocardial stress mouse model via preventing oxidative stress and apoptosis (17).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of carnosic acid against mitochondria‑mediated injury in H9c2 cardiomyocytes induced by hypoxia/reoxygenation

Liu

Dong

2017

Exp Ther Med

View full text Add to dashboard Cite

Abstract. Myocardial ischemia and reperfusion occurs in myocardial infarction. Timely reperfusion will exacerbate the injury through the mitochondria-mediated apoptosis in cardiomyocytes due to the accumulation of excessive reactive oxygen species (ROS). In order to identify novel therapeutic approaches, the cardioprotective effects of carnosic acid and the underlying mechanisms were investigated in the present study in H9c2 cardiomyocytes injured by hypoxia/reoxygenation in vitro. The viability of H9c2 cardiomyocytes was detected by MTT assay and further confirmed by the detection of intracellular lactate dehydrogenase (LDH) release. The mitochondrial function in H9c2 cardiomyocytes was evaluated using fluorescence methods. The proteins related to apoptosis, including caspase-3, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) were analyzed by western blot analysis, and the activity of caspase-3 was determined using a colorimetric method. As a result, carnosic acid was demonstrated to improve the viability of H9c2 cardiomyocytes and suppress the leakage of cytosolic lactate dehydrogenase under hypoxia/reoxygenation. In addition, the overproduction of intracellular ROS and intracellular calcium overload were ameliorated in the presence of carnosic acid. The dysfunction of mitochondria in H9c2 cardiomyocytes was also attenuated by carnosic acid through blocking the collapse of mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (mPTP) opening. Furthermore, the apoptosis of H9c2 cardiomyocytes resulted from hypoxia/reoxygenation was inhibited by carnosic acid through the upregulation of Bcl-2 and the downregulation of Bax and caspase-3 levels. These results provided evidence for further investigation that would assist in the development of novel therapeutic approaches for myocardial infarction.

show abstract

“…Considering all these reports, there is a clear body of evidence to support the potential of simultaneous activation of Nrf2 and eNOS as a therapeutic target in the prevention of cardiac diseases. [109] Maslinic acid Triterpene Coleus tuberosus [110] Triphlorethol-A Phlorotannin Ecklonia cava [111] Tanshinone IIA Phenanthrenequino ne Salvia miltiorrhiza [112] Schisandrin B Dibenzocyclooctad iene Saururus chinensis [113] α-Lipoic Acid Vicinal dimercaptans Vegetables and fruits [114] Sulforaphane Isothiocyanates …”

Section: Activators Of No-nrf2/are Pathway For the Protection Againstmentioning

confidence: 99%

Regression of Oxidative Stress by Targeting eNOS and Nrf2/ARE Signaling: A Guided Drug Target for Cardiovascular Diseases

Ramprasath¹,

Vasudevan²,

Sundaresan³

et al. 2015

CTMC

View full text Add to dashboard Cite

Cardiovascular diseases (CVDs) are the major health concern and the leading cause of death. Imbalance between free radicals and anti-oxidant defence is associated with cellular dysfunctions leading to the pathophysiology of various diseases including cardiac and vascular diseases. The stress responsive transcription factor NF-E2-related factor 2/antioxidant response element (Nrf2/ARE) regulates the expression of many detoxifying genes. Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is an important regulator of vascular function. Involvement of NO in modulating Nrf2 signaling is well established. Thus, it is apparent that increasing NO bioavailability and antioxidant status in vascular and myocardial tissue can be considered as a potential strategy to prevent the onset of vascular dysfunction and CVDs and is therefore of therapeutical interest. Based on the marked protective effect of Nrf2/ARE signalling and intriguing links between antioxidant mechanism and endothelial derived NO, the aim of the present review is to compile conclusive evidence for the involvement of NO-Nrf2/ARE axis in the regulation of cardiovascular function. This review also discusses on improving eNOS and Nrf2 signalling by Nrf2 activators which holds promise for countering cardiac and vascular disorders.

show abstract

Carnosic acid promotes myocardial antioxidant response and prevents isoproterenol-induced myocardial oxidative stress and apoptosis in mice

Cited by 43 publications

References 40 publications

Rosemary supplementation (Rosmarinus oficinallis L.) attenuates cardiac remodeling after myocardial infarction in rats

Rosemary supplementation (Rosmarinus oficinallis L.) attenuates cardiac remodeling after myocardial infarction in rats

Protective effects of carnosic acid against mitochondria‑mediated injury in H9c2 cardiomyocytes induced by hypoxia/reoxygenation

Regression of Oxidative Stress by Targeting eNOS and Nrf2/ARE Signaling: A Guided Drug Target for Cardiovascular Diseases

Contact Info

Product

Resources

About