Efficiency of Traditional Chinese medicine targeting the Nrf2/HO-1 signaling pathway.

Sulforaphane protects against skeletal muscle dysfunction in spontaneous type 2 diabetic db/db mice.

Hyperglycemia is associated with impairment of heart function. The current study aimed to investigate the ameliorative effect of polydatin-loaded chitosan nanoparticles (PD-CSNPs), polydatin (PD) and metformin (MET) on diabetic cardiomyopathy in rats. Rats divided into six groups; normal-control, diabetic-control, diabetic + CSNPs (diabetic rats treated with 50 mg/kg blank chitosan nanoparticles), diabetic + PD-CSNPs (diabetic rats treated with PD-CSNPs equivalent to 50 mg/kg of polydatin), diabetic + PD (diabetic rats given 50 mg/kg polydatin), diabetic + MET (diabetic rats given 100 mg/kg metformin), orally and daily for 4 weeks. Treatment of diabetic rats with PD-CSNPs, PD and MET showed a significant reduction in the values of glucose and glycosylated hemoglobin with improvement in heart function biomarkers through decreasing serum creatine kinase and creatine kinase myocardial band activities compared to diabetic control. The treatment agents also suppressed the elevated lipid peroxidation product, increased values of glutathione content, superoxide dismutase, superoxide peroxidase, and catalase activities in the heart of diabetic treated rats. Furthermore, PD-CSNPs, PD and MET decreased heart tissue levels of a pro-inflammatory cytokine; tumor necrosis factor-alpha and nuclear factor-kappa β, upregulation of heart gene expressions; nuclear factor erythroid 2-related factor 2 and heme oxygenase-1. Histological and ultrastructural examinations revealed the ameliorative effect of PD-CSNPs, PD and MET against the harmful of diabetic cardiomyopathy by reducing the cardiac fibers, necrotic cardiac myocytes, inflammatory cell infiltration, and the arrangement of the myofibrils and intercalated discs. In conclusion, the new formula of PD-CSNPs was more effective than PD and MET in amelioration the diabetic cardiomyopathy through its antioxidant, anti-inflammatory and prolonged-release properties.

Polydatin and polydatin-loaded chitosan nanoparticles attenuate diabetic cardiomyopathy in rats

Enhanced transdermal delivery of polydatin via a combination of inclusion complexes and dissolving microneedles for treatment of acute gout arthritis

Polydatin is a natural potent stilbenoid polyphenol and a resveratrol derivative with improved bioavailability. Polydatin possesses potential biological activities predominantly through the modulation of pivotal signaling pathways involved in inflammation, oxidative stress, and apoptosis. Various imperative biological activities have been suggested for polydatin towards promising therapeutic effects, including anticancer, cardioprotective, anti-diabetic, gastroprotective, hepatoprotective, neuroprotective, anti-microbial, as well as health-promoting roles on the renal system, the respiratory system, rheumatoid diseases, the skeletal system, and women’s health. In the present study, the therapeutic targets, biological activities, pharmacological mechanisms, and health benefits of polydatin are reviewed to provide new insights to researchers. The need to develop further clinical trials and novel delivery systems of polydatin is also considered to reveal new insights to researchers.

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Polydatin: Pharmacological Mechanisms, Therapeutic Targets, Biological Activities, and Health Benefits

Polydatin is a traditional Chinese medicine that provides myocardial protection after acute myocardial infarction (AMI) The study aim was to investigate the myocardial protection polydatin in H9c2 myocardial cells cultured in a hypoxic atmosphere and in a rat AMI model induced by ligating the left anterior descending coronary artery and treated with polydatin 100 mg/kg/day for 30 days The involvement of Nrf2 in mediating the effects of polydatin was investigated in H9c2 cells following Nrf2 knockdown by transfection of siRNA Polydatin suppressed hypoxia-induced H9c2 cell apoptosis and reactive oxygen species (ROS) generation by promoting Nrf2/HO-1 signaling Nrf2 knockdown reversed the protective effects of polydatin against hypoxia-induced myocardial cell injury The in vivo results were consistent with polydatin suppression of apoptosis and ROS generation in myocardial tissue by promotion of Nrf2/HO-1 signaling In conclusion, polydatin effectively inhibited hypoxia- and AMI-induced myocardial damage by promotion of Nrf2/HO-1 signaling

Dawei Cao

Papers

Polydatin protects against acute myocardial infarction-induced cardiac damage by activation of Nrf2/HO-1 signaling