Time filter

Source Type

Yao Y.-C.,Northeast Agricultural University | Yao Y.-C.,China Agricultural University | Yao Y.-C.,State Key Laboratories for Agrobiotechnology | Cai Z.-W.,Zhejiang University | And 6 more authors.
Hormone and Metabolic Research

It has been known that the changes in gonadal steroids are closely associated with adipose tissue metabolism. Domestic pigs have been a well-recognized experimental animal in biomedical research because of their similarity to humans in body size and other physiological/anatomical features. The aims of this study were to investigate the influence of castration-induced sex hormone deficiency on serum lipid levels and the genes expression of key enzymes associated with lipogenic and lipolytic processes in male pigs. The experimental animals consisted of 2 groups slaughtered on 147 th and 210 th day, respectively. In each of the group, 7 full-sib pairs of castrated and intact male hybrids from Yorkshire dams sired by Landrace were contained. The results showed that castration of male pigs led to increased total cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, and leptin levels in serum (p<0.05). No differences in levels of the free fatty acid, insulin, and glucose were observed between boars and barrows (p>0.05). Castration caused upregulation of fatty acid synthase and acetyl-CoA carboxylase alpha genes expression at both 147 and 210 days of age (p<0.05). No differences in expression of hormone sensitive lipase and adipose tissue triglyceride lipase genes were observed between boars and barrows at either 147 or 210 days of age (p>0.05). It is speculated that higher body fat deposition in castrated male pigs might have resulted mainly from increased transcription of the lipogenic genes, but not from decreased transcription of the lipolytic genes. © Georg Thieme Verlag KG Stuttgart · New York. Source

Shi F.,State Key Laboratories for Agrobiotechnology | Shi F.,Zhejiang University | Yang L.,State Key Laboratories for Agrobiotechnology | Wang J.,State Key Laboratories for Agrobiotechnology | And 6 more authors.
Acta Biochimica et Biophysica Sinica

The inflammatory responses in Alzheimer's disease and prion diseases are dominated by microglia activation. Three different phenotypes of microglial activation, namely classical activation, alternative activation, and acquired deactivation, have been described. In this study, we investigated the effect of amyloidogenic fragments of amyloid β and prion proteins (Aβ1-42 and PrP106-126) on various forms of microglial activation. We first examined the effect of Aβ1-42 and PrP106-126 stimulation on the mRNA expression levels of several markers of microglial activation, as well as the effect of cytochalasin D, a phagocytosis inhibitor, on microglial activation in Aβ1-42- and PrP106-126- stimulated BV2 microglia. Results showed that Aβ1-42 and PrP106-126 induced the classical activation of BV2 microglia, decreased the expression level of alternative expression markers, and had no effect on the expression of acquired deactivation markers. Cytochalasin D treatment significantly reduced Aβ1-42- and PrP106-126-induced up-regulation of proinflammatory factors, but did not change the expression profile of the markers of alternative activation or acquired deactivation in BV2 cells which were exposed to Aβ 1-42 and PrP106-126. Our results suggested that microglia interact with amyloidogenic peptides in the extracellular milieu-stimulated microglial classical activation and reduce its alternative activation, and that the uptake of amyloidogenic peptides from the extracellular milieu amplifies the classical microglial activation. © The Author 2013. Source

Song Z.,State Key Laboratories for Agrobiotechnology | Zhao D.,State Key Laboratories for Agrobiotechnology | Yang L.,State Key Laboratories for Agrobiotechnology
Acta Biochimica et Biophysica Sinica

Transmissible spongiform encephalopathies refer to a group of infectious neurodegenerative diseases with an entirely novel mechanism of transmission and pathophysiology including synaptic damage, dendritic atrophy, vacuolization, and microglial activation. Extensive neuronal loss is the main cause of chronic brain deterioration and fatal outcome of prion diseases. As the final outcome of pathological alterations, neuronal death is a prominent feature of all prion diseases. The mechanisms responsible for prion diseases are not well understood. A more comprehensive understanding of the molecular basis of neuronal damage is essential for the development of an effective therapy for transmissible spongiform encephalopathies and other neurodegenerative diseases sharing similar features. Here, we review the molecular mechanisms of mitochondrial dysfunction and endoplasmic reticulum stress-mediated neuronal death, which play crucial roles in the pathogenisis of prion diseases. © The Author 2013. Source

Yuan Z.,State Key Laboratories for Agrobiotechnology | Zhao D.,State Key Laboratories for Agrobiotechnology | Yang L.,State Key Laboratories for Agrobiotechnology
Acta Biochimica et Biophysica Sinica

Rabbits have low susceptibility to prion infection. Studies on prion protein (PrP) from animal species of different susceptibility to prion diseases identified key amino acid residues, specific motif, and special features in rabbit prion protein (RaPrPC) that contribute to the stability of rabbit PrPC and low susceptibility to prion infection. However, there is no evidence showing that rabbits are completely resistant to prion diseases. It has been reported that the rabbit prion could be generated in vitro through protein misfolding cyclic amplification and proved to be infectious and transmissible. Here, we reviewed studies on rabbitspecific PrP structures and features in relation to rabbit's low susceptibility to prion infection. © The Author 2013. Source

Discover hidden collaborations