Protection of plasma transfusion against lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure through inhibiting apoptosis of hepatic cells in mice

Fulminant hepatic failure is a severe clinical condition associated with extremely poor outcomes and high mortality. A number of studies have demonstrated the ability of plasma transfusion to successfully treat fulminant hepatic failure, but the underlying mechanisms are not well understood. The aim of the present study is to define the mechanisms of plasma transfusion treatment in lipopolysaccharide/D-galactosamine(LPS/D-Gal N)-induced mice. LPS/D-Gal N treatment in mice causes significant hepatic failure, including increasing serum aspartate aminotransferase(AST) and alanine aminotransferase(ALT) levels, histopathological changes in centrilobular necrosis and inflammatory cells, and the up-regulation of inflammation(tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6)). When LPS/D-Ga IN-induced mice were treated with plasma, these changes were halted. Results showed that plasma transfusion significantly reduced mortality, and decreased the levels of AST, ALT, and inflammation factors such as TNF-α and IL-6. The expression levels of cleaved Caspase-3, BAX, and p53 were down-regulated and Bcl-2 was up-regulated, suggesting that plasma can reduce LPS/D-Gal N-induced apoptosis. The protective mechanism of plasma against LPS/D-Gal N-induced fulminant hepatic failure is related to the inhibition of the inflammatory response and the reduction in apoptosis through the down-regulation of the p53-induced apoptotic pathway.

Cytotoxicity of anti-tumor herbal Marsdeniae tenacissimae extract on erythrocytes

Marsdeniae tenacissimae extract （MTE） has been used as an adjuvant medicine for cancer therapy for a long time. Although massive studies demonstrated its considerable anti-cancer effect, there is no research on its influence on erythrocytes, which are firstly interacted with MTE in the circulation. To investigate the influence of MTE on erythrocytes, we used a flow cytometer to detect the MTE-treated alternations of morphology, calcium concentration, and reactive oxygen species （ROS） level in erythrocytes. We used hemolysis under different osmotic solutions to evaluate the fragility of erythrocytes. Data showed that MTE treatment dose-dependently increased the ratio of erythrocyte fragmentation （P〈0.001） and shrinking, and elevated the forward scatter （FSC） value （P〈0.001） and calcium accumulation （P〈0.001）. MTE induced ROS production of erythrocytes under the high glucose condition （P〈0.01） and consequently caused a rise in fragility （P〈0.05）. These results suggest that MTE induces cytotoxicity and aging in erythrocytes in a dose-dependent manner, and presents the possibility of impairment on cancer patients＇ circulating erythrocytes when MTE is used as an anti-cancer adjuvant medicine.