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Fang X.,Suzhou University | Fang X.,Dalian University of Technology | Fang X.,Dalian SEM Bioengineer and Biotech Ltd. | Gao G.,Suzhou University | And 3 more authors.
Environmental Toxicology and Pharmacology | Year: 2012

This study investigated the toxic effects of perfluorononanoic acid (PFNA), a persistent organic pollutant, on rat hepatocytes and Kupffer cells in vitro and in vivo. The results showed that administration of 5μM PFNA increased the viabilities of the hepatocytes and the Kupffer cells. An exposure of 50μM PFNA did not alter the viabilities of both cells, as well as the release of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) from the primary cultured hepatocytes or the hepatocytes co-cultured with Kupffer cells. Anexposure of 100μM PFNA only decreased the viability of the hepatocytes. The administration of PFNA changed the hepatocyte expression of several genes related to lipid metabolism in vitro and in vivo. Oil Red O Staining revealed that 5mg PFNA/kg/D treatment lead to dramatic accumulation of lipids in rat liver. At the same dose PFNA damaged hepatocytes histopathologically. Up-regulated expressions of the inflammatory cytokines occurred in the Kupffer cells treated with 50μMPFNA and in the livers of the rat receiving a 5mg PFNA/kg/D treatment. In addition, these cytokines also increased in serum of the rat receiving higher dose of PFNA. In summary, on the one hand, PFNA exposure affected the viability of the hepatocytes, hepatic lipid metabolism and lead to lipid accumulation in liver. On the other hand, for the first time, PFNA exposure was demonstrated to affect the viability of the Kupffer cells aswell as their expression of cytokines, which involved in regulation of various liver functions. Therefore, we conclude that both the hepatocyte and the Kupffer cell contribute to the observed hepatotoxicity of PFNA. © 2012 Elsevier B.V. Source


Xue H.Y.,Suzhou University | Xue H.Y.,Dalian University of Technology | Xue H.Y.,Dalian SEM Bioengineer and Biotech Ltd. | Niu D.Y.,Dalian University of Technology | And 6 more authors.
Molecular Biology Reports | Year: 2011

In this study, the effect of aucubin on H2O2- induced apoptosis was studied by using a rat pheochromocytoma (PC12) cell line. We have analyzed the apoptosis of H2O2-induced PC12 cells, H 2O2-induced apoptosis appeared to correlate with lower Bcl-2 expression, higher Bax expression and sequential activation of caspase-3 leading to cleavage of poly-ADP-ribose polymerase (PARP). Aucubin not only inhibited lower Bcl-2 expression, high Bax expression, but also modulated caspase-3 activation, PARP cleavage, and eventually protected against H 2O2-induced apoptosis. These results indicated that aucubin can obstruct H2O2-induced apoptosis by regulating of the expression of Bcl-2 and Bax, as well as suppression of caspases cascade activation. © Springer Science+Business Media B.V. 2010. Source


Xue H.Y.,Suzhou University | Xue H.Y.,Dalian University of Technology | Xue H.Y.,Dalian SEM Bioengineer and Biotech Ltd. | Lu Y.N.,Dalian University of Technology | And 9 more authors.
Molecular Biology Reports | Year: 2012

In this study, we determined the neuroprotective effect of aucubin on diabetes and diabetic encephalopathy. With the exception of the control group, all rats received intraperitoneal injections of streptozotocin (STZ; 60 mg/kg) to induce type 1 diabetes mellitus (DM). Aucubin (1, 5, 10 mg/kg ip) was used after induction of DM (immediately) and diabetic encephalopathy (65 days after the induction of diabetes). The diabetic encephalopathy treatment groups were divided into short-term and long-term treatment groups. Treatment responses to all parameters were examined (body weight, plasma glucose, Y-maze error rates and proportion of apoptotic cells). In diabetic rats, aucubin controlled blood glucose levels effectively, prevented complications, and improved the quality of life of diabetic rats. In diabetic encephalopathy, aucubin significantly rescued neurons in the hippocampal CA1 subfield and reduced working errors during behavioral testing. The significant neuroprotective effect of aucubin could be seen not only in the short term (15 days) but also in the long term (45 days), which was a highly encouraging finding. These data suggest that aucubin may be a potential neuroprotective agent. © Springer Science+Business Media B.V. 2012. Source

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