Polydatin

1 Picea sp. 2 Polygonum sp. 3 Vitis sp.

Polydatin (Piceid), extracted from the roots of Polygonum cuspidatum Sieb, a widely used traditional Chinese remedies, possesses anti-inflammatory activity in several experimental models.

In Vitro:Polydatin protects cerebral cells from ischemic damages via improvement of microcirculation and inhibition of platelet aggregation. In addition, polydatin inhibits ICAM-1 expression in endothelial cells stimulated by lipopolysaccharide; it also attenuates adhesion between white blood cells and endothelial cells[1].

In Vivo:Polydatin could significantly increase the activity of SOD and the heart rate, attenuate myocardial pathological damage, decrease MDA content, slightly increase arterial pressure and GSH-Px activity, reduce intervals of QRS, QT and ST, and lower FFA content[2].

References:
[1]. Cheng Y, et al. Involvement of cell adhesion molecules in polydatin protection of brain tissues from ischemia-reperfusion injury. Brain Res. 2006 Sep 19;1110(1):193-200. [2]. Wang HL, et al. Synergistic effects of Polydatin and Vitamin C in Inhibiting Cardiotoxicity induced by Doxorubicin in rats. Fundam Clin Pharmacol. 2016 Nov 28. [Epub ahead of print] [3]. Jiang KF, et al. Polydatin ameliorates Staphylococcus aureus-induced mastitis in mice via inhibiting TLR2-mediated activation of the p38 MAPK/NF-κB pathway. Acta Pharmacol Sin. 2016 Nov 28. [Epub ahead of print]

Polydatin--a new mitochondria protector for acute severe hemorrhagic shock treatment.[Pubmed:23241098]

Expert Opin Investig Drugs. 2013 Feb;22(2):169-79.

OBJECTIVE: The aim of the study was find out whether neuronal mitochondrial injury does take place in severe shock and to explore effective therapy for severe shock. RESEARCH DESIGN AND METHODS: Rats were divided in the following group: sham, shock + normal saline (NS), shock + cyclosporine A (CsA), shock + resveratrol (Res) and shock + Polydatin (PD). Rats were subjected to shock for 2 h, followed by administration of NS, CsA, Res and PD, and infusion of shed blood. Morphology, metabolism and function of mitochondria were measured. RESULTS: Increased lipid peroxides (LPO) levels, lysosomal injury and mitochondrial permeability transition pore opening took place in neurons, resulting in swollen mitochondria with poorly defined cristae, decreased mitochondrial membrane potential (DeltaPsi) and reduced ATP content in shock + NS group, indicating mitochondrial dysfunction. Mitochondrial protectors, such as CsA, Res and PD, partially inhibited these alterations, especially following PD protection, ATP level increased from 44.14 +/- 13.81% in shock + NS group to 89.57 +/- 9.21% and the survival time was prolonged from 6.3 +/- 5.9 h in the shock + NS group to 31.6 +/- 13.7 h in shock + PD group. CONCLUSIONS: The study shows that neuronal mitochondrial injury is involved in the genesis of severe shock and PD may be the best choice for protection of neuron against mitochondrial injury in severe shock.

Polydatin inhibits growth of lung cancer cells by inducing apoptosis and causing cell cycle arrest.[Pubmed:24348867]

Oncol Lett. 2014 Jan;7(1):295-301.

Polydatin (PD), a small natural compound from Polygonum cuspidatum, has a number of biological functions. However, the anticancer activity of PD has been poorly investigated. In the present study, thiazolyl blue tetrazolium bromide assay was used to evaluate the inhibitory effect of PD on cell growth. Cell cycle distribution and apoptosis were investigated by flow cytometry. In addition, the expression of several proteins associated with apoptosis and cell cycle were analyzed by western blot analysis. The results demonstrated that PD significantly inhibits the proliferation of A549 and NCI-H1975 lung cancer cell lines and causes dose-dependent apoptosis. Cell cycle analysis revealed that PD induces S phase cell cycle arrest. Western blot analysis showed that the expression of Bcl-2 decreased as that of Bax increased, and the expression of cyclin D1 was also suppressed. The results suggest that PD has potential therapeutic applications in the treatment of lung cancer.

Effects of polydatin from Polygonum cuspidatum on lipid profile in hyperlipidemic rabbits.[Pubmed:18657948]

Biomed Pharmacother. 2009 Aug;63(7):457-62.

Hyperlipidemia is one of the vital coronary risk factors and is positively related to morbidity and mortality of coronary heart disease. There are numerous herbal medicines which are reported to exert good hypolipidemic actions with few side effects. In the present study, the hypolipidemic effects of Polydatin, a compound from Polygonum cuspidatum Sieb. et Zucc, on hyperlipidemic rabbits were evaluated. Thirty-two male rabbits were fed a high fat/cholesterol diet for 6 weeks and another eight male rabbits fed a basic diet served as normal control. Three weeks after a high fat/cholesterol diet, the animals were orally administrated Polydatin (25, 50, and 100 mg kg(-1) per day) by intubation for 3 weeks. The results showed that Polydatin markedly decreased the serum levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) in hyperlipidemic rabbits. The ratio of TC to high-density lipoprotein cholesterol (HDL-C) and the liver coefficient were also reduced. But both Polydatin and high fat/cholesterol diet did not evidently affect body weight in hyperlipidemic rabbits. All these results suggest that Polydatin from Polygonum cuspidatum has favorable potency to develop a hypolipemic and/or hepatoprotective agent in clinic. However the mechanism of hypolipemic action of Polydatin is in need of further clarity.

[Inhibitory effect of polydatin on expression of toll-like receptor 4 in ischemia-reperfusion injured NRK-52E cells].[Pubmed:25509306]

Zhongguo Zhong Yao Za Zhi. 2014 Aug;39(16):3157-61.

Polydatin is a monocrystaline compound isolated from Polygonum cuspidatum Sieb. et Zucc. (Polygonaceae) with biological properties, such as anti-inflammation, anti-oxidative and nephroprotective effects. Increasing number of studies have demonstrated the protective effect of Polydatin on renal ischemia reperfusion injury. However, the possible mechanisms of this protection are not fully elucidated. This study aimed to investigate the effect of Polydatin on ischemia-reperfusion induced expression of toll-like receptor4 (TLR4) in rat renal tubular epithelia cells (NRK-52E), and analyze the mechanism of Polydatin on TLR4 signal pathway. The cultured NRK-52E cells were incubated in three gas incubators for a period of 6 h at hypoxia and 24h at reoxygenation to simulate the ischemia-reperfusion injury in vitro. TLR4 mRNA level was analyzed by real-time-PCR, and the protein expression of TLR4 and NF-kappaB by Western blotting, while TNF-alpha and IL-1beta proteins expressions were detected by ELISA. Polydatin downregulated I/R induced mRNA and protein expressions of TLR4, and decreased the protein expression of NF-kappaB, TNF-alpha and IL-1beta. The TLR4 blocker partially antagonized the effect of I/R on NF-kappaB signaling, and such inhibitory effect was markedly enhanced by Polydatin. In the present study, Polydatin protects NRK-52E cells from I/R injury possibly by relieving the inflammatory response through regulation of TLR4/NF-kappaB signaling pathway.

Polydatin improves glucose and lipid metabolism in experimental diabetes through activating the Akt signaling pathway.[Pubmed:25310908]

Eur J Pharmacol. 2014 Dec 15;745:152-65.

Recently, the effect of Polydatin on lipid regulation has gained considerable attention. And previous study has demonstrated that Polydatin has hypoglycemic effect on experimental diabetic rats. Repressed Akt pathway contributes to glucose and lipid disorders in diabetes. Thus, whether Polydatin regulates glucose and lipid metabolism in experimental diabetic models through the Akt pathway arouses interest. The purpose was to explore the regulatory mechanism of polydain on glucose and lipid through Akt pathway. We used a diabetic rat model induced by high-fat and -sugar diet with low-dose of streptozocin and an insulin resistant HepG2 cell model induced by palmitic acid to clarify the role of Polydatin on glucose and lipid metabolism. Here, we found that Polydatin significantly attenuated fasting blood-glucose, glycosylated hemoglobin, glycosylated serum protein, total cholesterol, triglyceride, and low-density lipoprotein cholesterol in diabetic rats. Furthermore, Polydatin significantly increased glucose uptake and consumption and decreased lipid accumulation in insulin resistant HepG2 cells. Polydatin markedly increased serum insulin levels in diabetic rats, and obviously activated the Akt signaling pathway in diabetic rat livers and insulin resistant HepG2 cells. Polydatin markedly increased phosphorylated GSK-3beta, decreased the protein levels of G6Pase and SREBP-1c, and increased protein levels of GCK, LDLR, and phosphorylated IRS in livers and HepG2 cells. Overall, the results indicate that Polydatin regulates glucose and lipid metabolism in experimental diabetic models, the underlying mechanism is probably associated with regulating the Akt pathway. The effect of Polydatin on increased Akt phosphorylation is independent of prompting insulin secretion, but dependent of increasing IRS phosphorylation.

Polydatin modulates inflammation by decreasing NF-kappaB activation and oxidative stress by increasing Gli1, Ptch1, SOD1 expression and ameliorates blood-brain barrier permeability for its neuroprotective effect in pMCAO rat brain.[Pubmed:22001340]

Brain Res Bull. 2012 Jan 4;87(1):50-9.

Inflammation and oxidative stress play an important role in cerebral ischemic pathogenesis. Polydatin has been proved to elicit numerous biological effects through its anti-inflammatory and anti-oxidant properties. However, little is known regard to the mechanism of Polydatin's neuroprotection in ischemic stroke. We therefore investigated the potential neuroprotective effects of Polydatin and explored the underlying mechanisms. Male, Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (pMCAO). Experiment 1 was used to evaluate the expression of glioma-associated oncogene homolog1 (Gli1), Patched-1 (Ptch1) and Superoxide dismutase 1 (SOD1) after pMCAO, six time points were included. Experiment 2 was used to detect Polydatin's neuroprotection after pMCAO. Neurological deficit, brain water content and infarct size were measured at 24h and 72 h after pMCAO. Immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR), Western Blotting, activity assay and confocal microscope were used to analyse the expression of Gli1, Ptch1, SOD1 and nuclear factor-kappa B (NF-kappaB). Experiment 3 was used to detect Polydatin's influence on blood-brain barrier (BBB). Compared with Sham group, the expression of Gli1, Ptch1 and SOD1 were up-regulated shortly after pMCAO (P<0.05). Compared with Vehicle group, high dose of Polydatin (50mg/kg) up-regulated Gli1, Ptch1, SOD1 and down-regulated NF-kappaB, and reduced infarct volume, brain water content and behavioral deficits (P<0.05). Meanwhile, BBB permeability was also ameliorated. The results indicated that Polydatin protected the brain from damage caused by pMCAO, and this effect may be through up-regulating the expression of Gli1, Ptch1 and SOD1 and down-regulating the expression of NF-kappaB, and ameliorating BBB permeability.

Inhibitory Effects of Polydatin on Lipopolysaccharide-Stimulated RAW 264.7 Cells.[Pubmed:25567371]

Inflammation. 2015;38(3):1213-20.

The purpose of this study was to evaluate the effects of Polydatin (PD) on cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions at protein and transcriptional levels, as well as the production of prostaglandin E2 (PGE2) and nitric oxide (NO) in lipopolysaccharide (LPS)-induced macrophage RAW 264.7 cells. To elucidate the underlying mechanism responsible for these symptoms, we investigated the phosphorylation of mitogen-activated protein kinase (MAPK) pathway and nuclear factor-kappaB (NF-kappaB) expression. NO was analyzed with the Griess method. PGE2 was measured by enzyme-linked immunosorbent assay (ELISA). iNOS and COX-2 messenger RNA (mRNA) were identified by qPCR assay. iNOS, COX-2, NF-kappaB, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 protein expressions were detected with Western blot. The results revealed that PD effectively inhibited NO and PGE2 production, and it is not surprising that PD reduced iNOS and COX-2 expression at protein and transcriptional levels. Additionally, PD significantly ameliorated the activation of NF-kappaB and the phosphorylation of MAPKs in LPS-induced RAW 264.7 macrophages. These findings suggested that PD exerted potent anti-inflammatory activity in macrophages.

Protective effect of polydatin against ischemia/reperfusion injury in rat heart.[Pubmed:18425301]

Sheng Li Xue Bao. 2008 Apr 25;60(2):161-8.

The aim of the present study was to investigate the protective effect of Polydatin against myocardial ischemia/reperfusion injury in rats and the underlying mechanism. In anesthetized rats, ischemia and reperfusion arrhythmia produced by ligating and loosing the coronary artery was recorded and myocardial infarct size was measured. In Langendorff isolated rat heart, cardiac function was recorded before and after 30 min of global ischemia followed by 60 min of reperfusion. The parameters of cardiac function include left ventricular developed pressure (LVDP), maximal differentials of LVDP (+/-LVdp/dt(max)) and coronary flow (CF) were measured. Myocardial superoxide dismutase (SOD) activity, the contents of myocardial malondialdehyde (MDA) and nitric oxide (NO) as well as the activity of nitric oxide synthase (NOS) were measured in isolated heart. The results showed: (1) Arrhythmia score and myocardial infarct size were significantly lower in Polydatin group than that in the control group (P<0.05, P<0.01); (2) The recovery of LVDP, +/-LVdp/dt(max) and CF during reperfusion in Polydatin group were significantly better than that in the control rats (P<0.05, P<0.01); (3) SOD activity in Polydatin group was significantly higher than that in the control group, but MDA content was lower in Polydatin group than that in the control group (P<0.05); (4) NO content and NOS activity, especially constitutive nitric oxide synthase (cNOS) activity in Polydatin group were higher than that in the control group (P<0.05); (5) L-NAME, the NOS inhibitor, reversed the protective effect of Polydatin against ischemia/reperfusion injury. The results suggest that Polydatin has a protective effect against ischemia/reperfusion injury in rat heart. The cardioprotection of Polydatin is mainly mediated by cNOS which leading to an increase in NO production.

Polydatin (Piceid), extracted from the roots of Polygonum cuspidatum Sieb, a widely used traditional Chinese remedies, possesses anti-inflammatory activity in several experimental models.

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