Abstract:AIM To investigate the protective effects of polydatin (PD) against injury to primarily cultured rat hepatocytes induced by CCl4. METHODS Rat hepatocytes were separated by methods of liver infusion in vivo and cultured medium (7.5×10 5 cells/mL). Two mL or 0.2mL was added into 24-well or 96-well plates respectively. Twenty-four hours after cell preculture, PD at concentrations of 10 -7 mol/L-10 -4 mol/L was added into each plate. At the same time injury to hepatocytes was induced by adding 10mmol/L-CCl 4 . The… Show more
“…Polydatin (3,4′,5-trihydroxystibene 3-beta-mono-D-glucoside) (l " Fig. 1 A) has been widely studied because of its vast pharmacological activities, including inhibiting the production of inflammatory mediators [12], inducing production of antioxidants [13], regulating immune function [14], preventing mutations [15], inducing the apoptosis of tumor cells [16], protecting the liver [17] and preventing cardiovascular disease [18]. It has been demonstrated that the biomedical properties of resveratrol (trans-3,5,4′-trihydroxystilbene) are similar to those of polydatin as mentioned above despite their disparate polarities (l " Fig.…”
Nuclear factor- κB (NF- κB) plays a pivotal role in the regulation of immune and inflammatory responses. The real-time expression level of NF- κB reflects the development of ulcerative colitis (UC). Polydatin has vast pharmacological activities, including inhibiting the production of inflammatory mediators, inducing the production of antioxidants, regulating immune function, etc. The purpose of this study was to investigate the potential inhibitory effects of polydatin on NF- κB pathway activation in a mouse UC model. The results showed that polydatin treatment downregulated NF- κB p65 activity and expression, blocked the expression of TNF- α, IL-6 and IL-1 β at both mRNA and protein levels, decreased myeloperoxidase (MPO) activity, and alleviated inflammatory damage of colitis in mice with UC (p < 0.05), suggesting that the anti-inflammation effects of polydatin can be attributed, at least partially, to the blocking of the NF- κB pathway.
“…Polydatin (3,4′,5-trihydroxystibene 3-beta-mono-D-glucoside) (l " Fig. 1 A) has been widely studied because of its vast pharmacological activities, including inhibiting the production of inflammatory mediators [12], inducing production of antioxidants [13], regulating immune function [14], preventing mutations [15], inducing the apoptosis of tumor cells [16], protecting the liver [17] and preventing cardiovascular disease [18]. It has been demonstrated that the biomedical properties of resveratrol (trans-3,5,4′-trihydroxystilbene) are similar to those of polydatin as mentioned above despite their disparate polarities (l " Fig.…”
Nuclear factor- κB (NF- κB) plays a pivotal role in the regulation of immune and inflammatory responses. The real-time expression level of NF- κB reflects the development of ulcerative colitis (UC). Polydatin has vast pharmacological activities, including inhibiting the production of inflammatory mediators, inducing the production of antioxidants, regulating immune function, etc. The purpose of this study was to investigate the potential inhibitory effects of polydatin on NF- κB pathway activation in a mouse UC model. The results showed that polydatin treatment downregulated NF- κB p65 activity and expression, blocked the expression of TNF- α, IL-6 and IL-1 β at both mRNA and protein levels, decreased myeloperoxidase (MPO) activity, and alleviated inflammatory damage of colitis in mice with UC (p < 0.05), suggesting that the anti-inflammation effects of polydatin can be attributed, at least partially, to the blocking of the NF- κB pathway.
“…PD reduces lipid profile in hyperlipidemic rabbits (Xing et al, 2009) and exerts the neuroprotective effect on cerebral injury induced by ischaemia/reperfusion (Cheng et al, 2006). Also, it protects the primarily cultured rat hepatocytes against CCl 4 -induced injury (Huang et al, 1999) and reduces lipid oxidation (Pan et al, 2007). Nonetheless, there has been no report on the reproductive effect of PD on arsenic-induced toxicity in rats, yet.…”
Arsenic causes lipid peroxidation leading to alterations in antioxidant status in organisms. In this study, the reproductive effects of chronic exposure to arsenic and the protective effects of polydatin (PD) were evaluated in 35 Wistar male rats, which were divided equally into five groups. The control group received a normal diet and tap water, arsenic (100 mg l(-1) , approximately 1/50 of oral LD50 ) was given via drinking water to experimental groups except control group, and PD was orally given to the other groups at dose of 50, 100 and 200 mg kg(-1) for 60 days. Arsenic administration decreased sperm motility, glutathione level, superoxide dismutase and catalase activities in testicular tissue of rats. In contrast, malondialdehyde level and DNA damage were found to be high levels in arsenic-treated group. Histopathologically, it was observed that decreased sperm concentration and degeneration of Sertoli cells in testicular tissue. PD administration, partially 200 mg kg(-1) , reversed arsenic-induced lipid peroxidation, DNA damage, antioxidant enzyme activity and cell integrity in testis of rats. These results demonstrate that PD decreases arsenic-induced lipid peroxidation, enhances the antioxidant defence mechanism and regenerates tissue damage in testis of rats.
“…Polydatin exhibits favorable fall hematic fat action, which decreases the serum levels of total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C), reduces the content of hepatic TG, and depresses the ratios of LDL-C/high-density lipoprotein cholesterol (HDL-C) and TC/HDL-C in hyperlipidemic hamster [16] and rabbit models [17]. CCl 4 -induced rat hepatocyte injury in vitro can also be evidently alleviated by polydatin via regulation of SOD and MDA levels [18]. Nevertheless, there have been no reports on the protective effects of polydatin against liver injury in vivo, as far as we are aware.…”
Polydatin is one of main compounds in Polygonum cuspidatum, a plant with both medicinal and nutritional value. The possible hepatoprotective effects of polydatin on acute liver injury mice induced by carbon tetrachloride (CCl4) and the mechanisms involved were investigated. Intraperitoneal injection of CCl4 (50 µl/kg) resulted in a significant increase in the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and hepatic malondialdehyde (MDA), also a marked enhancement in the expression of hepatic tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and nuclearfactor-kappa B (NF-κB). On the other hand, decreased glutathione (GSH) content and activities of glutathione transferase (GST), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were observed following CCl4 exposure. Nevertheless, all of these phenotypes were evidently reversed by preadministration of polydatin for 5 continuous days. The mRNA and protein expression levels of hepatic growth factor-beta1 (TGF-β1) were enhanced further by polydatin. These results suggest that polydatin protects mice against CCl4-induced liver injury through antioxidant stress and antiinflammatory effects. Polydatin may be an effective hepatoprotective agent and a promising candidate for the treatment of oxidative stress- and inflammation-related diseases.
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