Antioxidative mechanism of Lycium barbarum polysaccharides promotes repair and regeneration following cavernous nerve injury.

Polysaccharides extracted from Lycium barbarum exhibit antioxidant properties. We hypothesized that these polysaccharides resist oxidative stress-induced neuronal damage following cavernous nerve injury. In this study, rat models were intragastrically administered Lycium barbarum polysaccharides for 2 weeks at 1, 7, and 14 days after cavernous nerve injury. Serum superoxide dismutase and glutathione peroxidase activities significantly increased at 1 and 2 weeks post-injury. Serum malondialdehyde levels decreased at 2 and 4 weeks. At 12 weeks, peak intracavernous pressure, the number of myelinated axons and nicotinamide adenine dinucleotide phosphate-diaphorase-positive nerve fibers, levels of phospho-endothelial nitric oxide synthase protein and 3-nitrotyrosine were higher in rats administered at 1 day post-injury compared with rats administered at 7 and 14 days post-injury. These findings suggest that application of Lycium barbarum polysaccharides following cavernous nerve crush injury effectively promotes nerve regeneration and erectile functional recovery. This neuroregenerative effect was most effective in rats orally administered Lycium barbarum polysaccharides at 1 day after cavernous nerve crush injury.

The role of human endogenous retroviral long terminal repeat sequences in human cancer (Review).

Human endogenous retrovirus (HERV) and solitary long terminal repeats (LTRs) constitute 8% of the human genome. Although most HERV genes are partially deleted and not intact, HERV LTRs comprise features including promoters, enhancers, selective splicer sites and polyadenylation sites in order to regulate the expression of neighboring genes. Owing to the genetic instability of LTRs, their wide distributions along human chromosomes are not only non-random, but are also correlated with gene density. Considerable evidence indicates that HERV LTRs regulate the expression of their adjacent viral and cellular genes in placental development and tumorigenesis. However, the regulatory mechanism of HERV LTRs on the expression of its neighboring cancer-associated genes in human cancers remains to be elucidated. Insertional mutagenesis, recombination and polymorphism are three principal factors of LTR that contribute to its genetic instability. Moreover, genetic instability, hypomethylation, transactivation and the antisense transcript of LTRs enhance the activity of LTRs and regulate the expression of their adjacent genes in human cancers. Therefore, in the present review, we examined the mechanism of HERV LTRs in tumorigenesis in combination with the structure and function of LTRs.