Coating function and stabilizing effects of surface layer protein from Lactobacillus acidophilus ATCC 4356 on liposomes.

Surface layer proteins (SLPs) are crystalline arrays in the outermost layer of cell envelope in many archaea and bacteria. SLPs subunits have the ability to reassemble on the surface of lipid layers. In this work, the SLP from Lactobacillus acidophilus ATCC 4356 was extracted and reassembled on the surface of positively charged liposomes composed of dipalmitoyl phosphatidylcholine, cholesterol and octadecylamine. Zeta potentials and particle size were determined to describe the adsorption process of SLP on liposomes. The liposomes completely coated with SLP were observed by transmission electron microscope. To investigate the stabilizing effects of SLP on liposomes, carboxyfluorescein (CF) was encapsulated and its leakage was determined as an evaluation index. The results showed that the L. acidophilus ATCC 4356 SLP significantly (P < 0.05) increased the stability of the liposomes in the course of thermal challenge. Furthermore, SLP was able to reduce the aggregation of liposomes in serum. Storage stability of liposomes was performed at 25 °C, 4 °C and -20 °C for 90 days. And the SLP-coated liposomes released less CF than the control liposomes during storage at the three evaluated temperatures. Our findings extended the application field of Lactobacillus SLPs and introduced a novel nanocarrier system with good chemical stability.

Disodium Guanylate Alleviates Acute Hepatic Injury Induced by Carbon Tetrachloride Via Antioxidative Stress and Antiapoptosis In Vivo and In Vitro.

Hepatic injury is one of the most common digestive system diseases worldwide in clinic. Guanylic acid or guanosine monophosphate (GMP) was an important component of nucleotides, which is mainly in the form of sodium salt (disodium guanylate, GMP-Na2 ). However, its effect on hepatic injury has not yet been investigated. This study is to investigate the protective effects of GMP-Na2 on acute hepatic injury induced by carbon tetrachloride (CCl4 ), and to explore its mechanism. The hepatic injury models of mice and HL-7702 cells were induced by CCl4 . The alanine transaminase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), total antioxidant capacity (T-AOC) were determined by biochemical method. Hematoxylin-eosin staining were used to determine the morphological changes on liver tissue in mice. The mRNA and protein expressions of caspase-3, Bax, and Bcl-2 were detected by RT-PCR and Western blot analysis. Our results show that GMP-Na2 treatment significantly decreased the activities of ALT and AST, and the levels of MDA as well as increased the levels of SOD, GSH-Px, and T-AOC. Importantly, GMP-Na2 effectively enhanced the antiapoptosis function by upregulating Bcl-2 expression and downregulating caspase-3 and Bax expressions in vivo and in vitro. Moreover, the histopathological changes of liver tissue were obviously improved after GMP-Na2 treatment. These findings suggest that GMP-Na2 has protective effects on hepatic injury, and its mechanisms may be associated with antioxidative stress and antiapoptosis.

A novel, ultra-large xylanolytic complex (xylanosome) secreted by Streptomyces olivaceoviridis.

The production of a novel, very large xylanolytic complex (xylanosome) by Streptomyces olivaceoviridis E-86 is reported. The molecular weight was approx. 1200 kDa as determined by native gradient gel electrophoresis. Corncob xylan was the best inducer of xylanosome formation. The xylanosome was produced when the organism was grown for 5 d between pH 4.5-6 and at 27.5 to 35 degrees C.