Analysis the alteration of systemic inflammation in old and young APP/PS1 mouse.

The impairment of cognitive function was considered as a major clinic feature in Alzheimer's disease (AD) patients. Thus, a number of researches related to AD were focused on the changes in brain. However, as a neurodegenerative disorder with systemic inflammation, the periphery organs may also play a key role in AD pathology. Here, we pose the hypothesis that histopathology and inflammatory response of periphery organs may alter with aging in APP/PS1 mouse model. Therefore, we performed immunohistochemical staining technology to double label Aß plaques and microglia cells in brain. The H&E staining was performed in periphery tissues and the mRNA expression of inflammatory factors IL-6, IL-10 and TNF-α were also determined. Next, the index of oxidative stress was measured. Consequently, the level of inflammatory factors was significantly increased in 24 months APP/PS1 mice. Furthermore, the enzyme activity of SOD, CAT and GSH were significantly decreased in colon and other organs. Our results demonstrated the increased inflammation response and declined antioxidative capacity of periphery organs in aged APP/PS1 mice, which suggesting that a more comprehensive perspective to study AD were necessary.

Association of anti-oxidative capacity of HDL with subclinical atherosclerosis in subjects with and without non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) patients are at a substantial risk for developing cardiovascular disease (CVD). High-density lipoprotein (HDL) is well known to have protective effects against the development of atherosclerotic CVD. One of the major antiatherogenic effects of HDL is its anti-oxidative function. OBJECTIVES: This study investigated the association of anti-oxidative capacity of HDL with subclinical atherosclerosis in NAFLD and non-NAFLD subjects. METHODS: A total of 143 subjects including 51 NAFLD and 92 control subjects were included in this case-control study. HDL oxidative index (HOI) was determined spectrophotometrically using a cell-free method in the presence of a fluorescent substrate dichlorofluorescein diacetate (DCFDA). Paraoxonase 1 (PON1) activity, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) plasma levels were assessed in both groups. RESULTS: The NAFLD patients with impaired HDL anti-oxidative function (HOI ≥ 1) had higher MDA levels, aspartate amino transferase (AST), liver stiffness (LS), and carotid intima-media thickness (cIMT) values compared to the controls. HDL oxidative index (HOI) was positively correlated with MDA levels and cIMT and negatively correlated with SOD activity. CONCLUSIONS: Higher circulating levels of MDA were associated with the impaired anti-oxidative function of HDL in NAFLD. The impaired anti-oxidative capacity of HDL might be related to NAFLD severity and subclinical atherosclerosis in NAFLD patients.

Recovery from discrete wound severities in side-blotched lizards (Uta stansburiana): implications for energy budget, locomotor performance, and oxidative stress.

Wounding events (predation attempts, competitive combat) result in injuries and/or infections that induce integrated immune responses for the recovery process. Despite the survival benefits of immunity in this context, the costs incurred may require investment to be diverted from traits contributing to immediate and/or future survival, such as locomotor performance and oxidative status. Yet, whether trait constraints manifest likely depends on wound severity and the implications for energy budget. For this study, food intake, body mass, sprint speed, and oxidative indices (reactive oxygen metabolites, antioxidant capacity) were monitored in male side-blotched lizards (Uta stansburiana) healing from cutaneous wounds of discrete sizes (control, small, large). Results indicate that larger wounds induced faster healing, reduced food consumption, and led to greater oxidative stress over time. Granted wounding did not differentially affect body mass or sprint speed overall, small-wounded lizards with greater wound area healed had faster sprint speeds while large-wounded lizards with greater wound area healed had slower sprint speeds. During recovery from either wound severity, however, healing and sprint performance did not correspond with food consumption, body mass loss, nor oxidative status. These findings provide support that energy budget, locomotor performance, and oxidative status of a reptile are linked to wound recovery to an extent, albeit dependent on wound severity.

Cytotoxicity studies of Fe3O4 nanoparticles in chicken macrophage cells.

Magnetic Fe3O4 nanoparticles (Fe3O4-NPs) have been widely investigated for their biomedical applications. The main purpose of this study was to evaluate the cytotoxic effects of different sizes of Fe3O4-NPs in chicken macrophage cells (HD11). Experimental groups based on three sizes of Fe3O4-NPs (60, 120 and 250 nm) were created, and the Fe3O4-NPs were added to the cells at different doses according to the experimental group. The cell activity, oxidative index (malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen species (ROS)), apoptosis and pro-inflammatory cytokine secretion level were detected to analyse the cytotoxic effects of Fe3O4-NPs of different sizes in HD11 cells. The results revealed that the cell viability of the 60 nm Fe3O4-NPs group was lower than those of the 120 and 250 nm groups when the same concentration of Fe3O4-NPs was added. No significant difference in MDA was observed among the three Fe3O4-NP groups. The SOD level and ROS production of the 60 nm group were significantly greater than those of the 120 and 250 nm groups. Furthermore, the highest levels of apoptosis and pro-inflammatory cytokine secretion were caused by the 60 nm Fe3O4-NPs. In conclusion, the smaller Fe3O4-NPs produced stronger cytotoxicity in chicken macrophage cells, and the cytotoxic effects may be related to the oxidative stress and apoptosis induced by increased ROS production as well as the increased expression of pro-inflammatory cytokines.