Polydatin prevents angiotensin II-induced cardiac hypertrophy and myocardial superoxide generation

Zhang, Qi; Tan, Yingying; Zhang, Nan; Yao, Fanrong

doi:10.1177/1535370214561958

Cited by 19 publications

(18 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The further studies show that polydatin protects against cardiac ischemia–reperfusion injury by modulating renin-angiotensin system and reducing ROS production [ 22 – 24 ], attenuates the cardiac dysfunction generated by burn through inhibiting ryanodine receptors [ 25 ], and alleviates cardiac dysfunction and mitochondrial function in the diabetic model [ 26 ]. In line with above findings, our study shows that polydatin protects against angiotensin II-induced cardiac hypertrophy both in vitro and in vivo through suppression of NADPH oxidase activity and superoxide production [ 27 ]. In addition, our previous studies have also shown that polydatin inhibits insulin resistance and improves hepatic steatosis [ 28 ].…”

Section: Introductionsupporting

confidence: 83%

Cardioprotective effects of polydatin against myocardial injury in diabetic rats via inhibition of NADPH oxidase and NF-κB activities

Tan

Chen

Fang

et al. 2020

BMC Complement Med Ther

Self Cite

View full text Add to dashboard Cite

Background Diabetic cardiomyopathy is a main cause of the increased morbidity in diabetic patients, no effective treatment is available so far. Polydatin, a resveratrol glucoside isolated from the Polygonum cuspidatum, was found by our and others have antioxidant and cardioprotective activities. Therapeutic effects of polydatin on diabetic cardiomyopathy and the possible mechanisms remains unclear. This study aimed to investigate the cardioprotective effects and underlying mechanisms of polydatin on myocardial injury induced by hyperglycemia. Methods Diabetes in rats was made by high-fat diet combined with multiple low doses of streptozotocin, and then treated with polydatin (100 mg·kg-1·day-1, by gavage) for 8 weeks. Cardiac function was examined by echocardiography. Myocardial tissue and blood samples were collected for histology, protein and metabolic characteristics analysis. In cultured H9c2 cells with 30 mM of glucose, the direct effects of polydatin on myocyte injury were also observed. Results In diabetic rats, polydatin administration significantly improved myocardial dysfunction and attenuated histological abnormalities, as evidenced by elevating left ventricular shortening fraction and ejection fraction, as well as reducing cardiac hypertrophy and interstitial fibrosis. In cultured H9c2 cells, pretreatment of polydatin dose-dependently inhibited high glucose-induced cardiomyocyte injury. Further observation evidenced that polydatin suppressed the increase in the reactive oxygen species levels, NADPH oxidase activity and inflammatory cytokines production induced by hyperglycemia in vivo and in vitro. Polydatin also prevented the increase expression of NOX4, NOX2 and NF-κB in the high glucose -stimulated H9c2 cells and diabetic hearts. Conclusions Our results demonstrate that the cardioprotective effect of polydatin against hyperglycemia-induced myocardial injury is mediated by inhibition of NADPH oxidase and NF-κB activity. The findings may provide a novel understanding the mechanisms of the polydatin to be a potential treatment of diabetic cardiomyopathy.

show abstract

Section: Introductionsupporting

confidence: 83%

Cardioprotective effects of polydatin against myocardial injury in diabetic rats via inhibition of NADPH oxidase and NF-κB activities

Tan

Chen

Fang

et al. 2020

BMC Complement Med Ther

Self Cite

View full text Add to dashboard Cite

show abstract

“…PD possesses antioxidative and anti‐inflammatory activities (Mohan et al, ). Previous studies have demonstrated the therapeutic effects of PD in HG‐induced injury in multiple organs, including heart, liver, and brain (Xu et al, ; Zhang, Tan, Zhang, & Yao, ). To test the safety of PD, we administered a single large PD dose of 5000 mg/kg body weight to mice and observed no adverse effects.…”

Section: Discussionmentioning

confidence: 99%

“…PD has been shown to possess antioxidant and anti‐inflammatory activities (Mohan et al, ). Previous studies have demonstrated the therapeutic effects of PD on HG‐induced injury in multiple organs, including the heart, liver, and brain (Xu et al, ; Zhang et al, ). In the present study, we observed that PD decreased all of the analyzed markers of renal dysfunction (Table ) in KKAy mice, suggesting that PD possesses renoprotective effects.…”

Section: Discussionmentioning

confidence: 99%

Polydatin impairs mitochondria fitness and ameliorates podocyte injury by suppressing Drp1 expression

Zheng

Tao

et al. 2017

Journal Cellular Physiology

View full text Add to dashboard Cite

Polydatin (PD), a resveratrol glycoside, has been shown to protect renal function in diabetic nephropathy (DN), but the underlying molecular mechanism remains unclear. This study demonstrates that PD stabilize the mitochondrial morphology and attenuate mitochondrial malfunction in both KKAy mice and in hyperglycemia (HG)‐induced MPC5 cells. We use Western blot analysis to demonstrate that PD reversed podocyte apoptosis induced by HG via suppressing dynamin‐related protein 1 (Drp1). This effect may depend on the ability of PD to inhibit the generation of cellular reactive oxygen species (ROS). In conclusion, we demonstrate that PD may be therapeutically useful in DN, and that, podocyte apoptosis induced by HG can be reversed by PD through suppressing Drp1 expression.

show abstract

“…Overall, the existing literature referencing resveratrol and Ang II in whole animal studies is surprisingly sparse. Polydatin, a resveratrol glucoside, was delivered in an Ang II-induced model of hypertension by Zhang et al, 26 who found that the chronic infusion of Ang II significantly increased systolic blood pressure from 120±3 to 162±7 mmHg with Ang II, and oral administration of polydatin for 5 weeks did not decrease the pressor effect of Ang II. Dolinsky et al 3 implanted mice with osmotic minipumps to deliver Ang II (1.4 mg/kg/d) and placed mice on a diet containing resveratrol (using ~320 mg/kg/d resveratrol).…”

Section: Discussionmentioning

confidence: 99%

Chronic resveratrol reverses a mild angiotensin II-induced pressor effect in a rat model

Gordish

Beierwaltes

2016

IBPC

View full text Add to dashboard Cite

Resveratrol is reported to reduce blood pressure in animal models of hypertension, but the mechanisms are unknown. We have shown that resveratrol infusion increases sodium excretion. We hypothesized that chronic ingestion of resveratrol would reduce angiotensin II (Ang II)-induced increases in blood pressure by decreasing oxidative stress and by also decreasing sodium reabsorption through a nitric oxide-dependent mechanism. We infused rats with vehicle or 80 μg Ang II/d over 4 weeks. Vehicle or Ang II-infused rats were individually housed, pair fed, and placed on a diet of normal chow or normal chow plus 146 mg resveratrol/d. Groups included 1) control, 2) resveratrol-fed, 3) Ang II-treated, and 4) Ang II plus resveratrol. Systolic blood pressure was measured by tail cuff. During the 4th week, rats were placed in metabolic caging for urine collection. NO2/NO3 and 8-isoprostane excretion were measured. Ang II increased systolic blood pressure in the 1st week by +14±5 mmHg (P<0.05) in Group 3 and +10±3 mmHg (P<0.05) in Group 4, respectively. Blood pressure was unchanged in Groups 1 and 2. After 4 weeks, blood pressure remained elevated in Group 3 rats with Ang II (+9±3 mmHg, P<0.05), but in Group 4, blood pressure was no longer elevated (+2±2 mmHg). We found no significant differences between the groups in sodium excretion or cumulative sodium balance (18.49±0.12, 17.75±0.16, 17.97±0.17, 18.46±0.18 μEq Na+/7 d in Groups 1–4, respectively). Urinary excretion of NO2/NO3 in the four groups was 1) 1631±207 μmol/24 h, 2) 1045±236 μmol/24 h, 3) 1490±161 μmol/24 h, and 4) 609±17 μmol/24 h. 8-Isoprostane excretion was 1) 63.85±19.39 nmol/24 h, 2) 73.57±22.02 nmol/24 h, 3) 100.69±37.62 nmol/24 h, and 4) 103.00±38.88 nmol/24 h. We conclude that chronic resveratrol supplementation does not blunt Ang II-increased blood pressure, and while resveratrol has mild depressor effects, these do not seem to be due to natriuresis or enhanced renal nitric oxide synthesis.

show abstract

Polydatin prevents angiotensin II-induced cardiac hypertrophy and myocardial superoxide generation

Cited by 19 publications

References 37 publications

Cardioprotective effects of polydatin against myocardial injury in diabetic rats via inhibition of NADPH oxidase and NF-κB activities

Cardioprotective effects of polydatin against myocardial injury in diabetic rats via inhibition of NADPH oxidase and NF-κB activities

Polydatin impairs mitochondria fitness and ameliorates podocyte injury by suppressing Drp1 expression

Chronic resveratrol reverses a mild angiotensin II-induced pressor effect in a rat model

Contact Info

Product

Resources

About