Activation of ALDH2 with Low Concentration of Ethanol Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetes Rat Model

Kang, Pan; Wu, Wenjuan; Tang, Yang; Xuan, Ling; Guan, Shu‐Hong; Tang, Bi; Zhang, Heng; Gao, Qin; Wang, Hongju

doi:10.1155/2016/6190504

Cited by 25 publications

(20 citation statements)

References 42 publications

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“…Furthermore, we found that daidzin (an ALDH2 antagonist) abolished baicalin‐exhibited beneficent effects against H/R‐induced cytotoxicity and apoptosis in H9c2 cells, and Alda‐1 (an ALDH2 agonist) also reversed H/R‐induced cytotoxicity and apoptosis. These results were in accordance with these studies whereby the modulation of ALDH2 activity by daidzin or Alda‐1 could affect myocardial apoptosis caused by I/R or H/R injury in isolated hearts and in cells . These results suggested that enhancing of ALDH2 activity and expression mediated H/R injury and the protective effects of baicalin against H/R injury in H9c2 cells.…”

Section: Discussionsupporting

confidence: 91%

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Baicalin protects H9c2 cardiomyocytes against hypoxia/reoxygenation‐induced apoptosis and oxidative stress through activation of mitochondrial aldehyde dehydrogenase 2

Jiang

Zhao

Chen

et al. 2017

Clin Exp Pharma Physio

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Baicalin, a flavonoid glycoside separated from Scutellaria baicalensis, has cardioprotection against ischaemia/reperfusion (I/R) injury. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is considered as an endogenous protective mechanism against I/R injury depending on its anti-oxidant and anti-apoptotic characteristics. The present study demonstrates whether ALDH2 contributes to the cardioprotection of baicalin against hypoxia/reoxygenation (H/R)-inudced H9c2 cardiomyocytes injury. Our results observed that H/R treatment resulted in a significant decrease in cells viability and obvious increases in caspase-3 activity and apoptosis rate in H9c2 cells, while these alterations were evidently reversed by baicalin pretreatment. Simultaneously, baicalin mitigated H/R-induced the decreases in the levels of ALDH2 mRNA and protein as well as the activity of ALDH2 in H9c2 cells. However, we found that daidzin, an ALDH2 antagonist, remarkably attenuated baicalin-elicited inhibitory action on H/R-induced the downregulation of cells viability and Bcl-2 protein expression, and the upregulations of caspase-3 activity, apoptosis rate, cytochrome c and Bax proteins expressions in H9c2 cells. In addition, baicalin reversed H/R-induced oxidative stress as evidenced by the downregulation of malondialdehyde (MAD) and 4-hydroxy aldehydes (4-HNE) levels, the inhibition of endogenous reactive oxygen species (ROS) generation, and the downregulation of superoxide dismutase (SOD) activity induced by H/R treatment, while these effects were also blocked by daidzin. Furthermore, we found that Alda-1, an ALDH2 agonist, also abolished H/R-induced cytotoxicity, apoptosis, and oxidative stress, indicating that ALDH2 mediated H/R-induced H9c2 cell injury. Overall, these results suggested that baicalin prevents H/R-induced apoptosis and oxidative stress through enhancing ALDH activity and expression in H9c2 cardiomyocytes.

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Section: Discussionsupporting

confidence: 91%

“…H/R, hypoxia/reoxygenation activity by daidzin or Alda-1 could affect myocardial apoptosis caused by I/R or H/R injury in isolated hearts and in cells. 24,35,36 These results suggested that enhancing of ALDH2 activity and expression mediated H/R injury and the protective effects of baicalin against H/R injury in H9c2 cells.…”

Section: Discussionmentioning

confidence: 76%

Baicalin protects H9c2 cardiomyocytes against hypoxia/reoxygenation‐induced apoptosis and oxidative stress through activation of mitochondrial aldehyde dehydrogenase 2

Jiang

Zhao

Chen

et al. 2017

Clin Exp Pharma Physio

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“…Chronic consumption of alcohol may lead to an increase in their activity/expression in the brain 42 . A recent study found that the cardioprotective effect of LAC is related to an upregulated ALDH2 18 . In the future, it will be important to determine the mechanisms by which LAC protects the brain against its post-ischemic inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have investigated the effect of alcohol consumption on cardiovascular diseases. Most studies have focused on the effects of binge drinking, however, some have sought to determine an association between light-moderate alcohol consumption and cardioprotection 17 , 18 . There have also been a limited amount of studies investigating the protective effects of low-dose alcohol on cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

Effect of Low-Dose Alcohol Consumption on Inflammation Following Transient Focal Cerebral Ischemia in Rats

McCarter

Jiang

et al. 2017

Sci Rep

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Increasing evidence suggest that low-dose alcohol consumption (LAC) reduces the incidence and improves the functional outcome of ischemic stroke. We determined the influence of LAC on post-ischemic inflammation. Male Sprague-Dawley rats were divided into 3 groups, an ethanol (13.5% alcohol) group, a red wine (Castle Rock Pinot Noir, 13.5% alcohol) group, and a control group. The amount of alcohol given to red wine and ethanol groups was 1.4 g/kg/day. After 8 weeks, the animals were subjected to a 2-hour middle cerebral artery occlusion (MCAO) and sacrificed at 24 hours of reperfusion. Cerebral ischemia/reperfusion (I/R) injury, expression of adhesion molecules and pro- and anti-inflammatory cytokines/chemokines, microglial activation and neutrophil infiltration were evaluated. The total infarct volume and neurological deficits were significantly reduced in red wine- and ethanol-fed rats compared to control rats. Both red wine and ethanol suppressed post-ischemic expression of adhesion molecules and microglial activation. In addition, both red wine and ethanol upregulated expression of tissue inhibitor of metalloproteinases 1 (TIMP-1), downregulated expression of proinflammatory cytokines/chemokines, and significantly alleviated post-ischemic expression of inflammatory mediators. Furthermore, red wine significantly reduced post-ischemic neutrophil infiltration. Our findings suggest that LAC may protect the brain against its I/R injury by suppressing post-ischemic inflammation.

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“…1,2 Diabetes is the most common reason for endstage heart disease. 3 The data from the World Health Organization (WHO) shows that about 347 million people around the world have diabetes, which is predicted to rank seventh in terms of leading death caused by the year 2030. 4 Blindness, kidney failure, as well as lower limb amputation, are demonstrated to be complications for diabetes.…”

Section: Introductionmentioning

confidence: 99%

Interfering with long chain noncoding RNA ANRIL expression reduces heart failure in rats with diabetes by inhibiting myocardial oxidative stress

Dai

Lee

2019

J of Cellular Biochemistry

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This study is performed to elucidate whether long‐chain noncoding RNA ANRIL has an effect on diabetes, and further explore the mechanism of ANRIL in diabetes. The rat model of diabetes was established via intraperitoneal injection of streptozotocin. The modeled rats were grouped into normal, diabetes, siRNA‐NC, and ANRIL siRNA groups. Besides, the expression of ANRIL, cardiac function, inflammatory factor levels, cardiomyocyte apoptosis, and levels of oxidative stress index were all determined. Upregulated ANRIL was found in myocardial tissue of diabetic rats. Downregulated ANRIL improved cardiac function index and the expression of inflammatory factors, improved the pathological state of myocardial tissue and myocardial remodeling, decreased myocardial collagen deposition area and cardiomyocyte apoptosis and reduced the oxidative level of myocardial tissue in diabetic rats. This present study suggests that upregulated ANRIL is found in myocardial tissue of diabetic rats. Additionally, silencing of ANRIL reduces myocardial injury in diabetes by inhibiting myocardial oxidative stress.

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Activation of ALDH2 with Low Concentration of Ethanol Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetes Rat Model

Cited by 25 publications

References 42 publications

Baicalin protects H9c2 cardiomyocytes against hypoxia/reoxygenation‐induced apoptosis and oxidative stress through activation of mitochondrial aldehyde dehydrogenase 2

Baicalin protects H9c2 cardiomyocytes against hypoxia/reoxygenation‐induced apoptosis and oxidative stress through activation of mitochondrial aldehyde dehydrogenase 2

Effect of Low-Dose Alcohol Consumption on Inflammation Following Transient Focal Cerebral Ischemia in Rats

Interfering with long chain noncoding RNA ANRIL expression reduces heart failure in rats with diabetes by inhibiting myocardial oxidative stress

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