Alzheimer's disease (AD) is a most common neurodegenerative disease. The mechanisms underlying AD, especially late-onset AD, remain elusive. In the past few years, results from genome-wide association studies (GWAS) and systems approaches indicated that innate immune responses mediated by microglia played critical roles in AD. Functional analysis on animal models also showed that immune receptors or proteins expressed in microglia mediated Abeta-induced inflammation, or Abeta phagocytosis by microglia. Microglia plays double sword roles in AD. More work is warranted to elucidate the exact roles of microglia in AD, which will facilitate our better understanding of the mechanisms underlying AD.

Objective To study the distribution and changes of three NOS isoforms in mouse uterus during reproductive stage and understand the possible physiological regulatory roles of endogenous NO in reproduction. Methods Immunohistochemisty and colorimetry were used. Results During reproductive stage, nNOS had a relatively stable expresstion in mouse uterus. Numerous positive cells mainly distributed in endometrial epithelium, endometrial stroma, glandular epithelium, vascular endothelium and smooth muscle. In the middle stage of pregnancy,eNOS had a significantly increased expresstion in mouse uterus. Strongly positive staining was observed in decidual epithelium, glandular epithelium and vascular endothelium. During early stage of pregnancy, iNOS had a relatively stronger expresstion in mouse uterus. Positve materia mainly located in smooth muscle, vascular endothelium, glandular epithelium and endometrial stromal cells. However, during estrus, the staining of iNOS in mouse uterus was negative. Moreover, the levels of NO in mouse serum during reproductive period were measured.Conclution During reproductive stage, three NOS isofoms may act dependently and independently. Endogenous NO may have physiological regulatory roles to estrogenicity, embryo implantation, maintaining the quiescence of the uterus before patrition and tissue remodelling after patrition of mice.\;[

Objective To understand the distribution of iNOS in the ovary, oviduct and uterus of mouse(2 5 days of pregnancy). Methods Immunohistochemistry(LSAB) was used in this study. Results iNOS occured in the luteal cells of all detected ovaries. In the oviduct tissues, iNOS was only found in the mucosa. It also appeared in the epithelia of endometrium and the metrial glands of all detected uterus. In the decidua of both day 4 and day 5 pregnant mice and the day 5 embryo surface, there are the presence of iNOS. Conclusion iNOS can be found in the ovaries,oviducts and uterus during 2 5days of pregnant mice, which suggests that iNOS plays a role in the development of early mouse embryos and the implantation.

Objective To detect the changes of immune cells in mouse uterus induced by SA 30(a Con A binding glycoprotein isolated from bovine sperms), and then reveal the influence of SA 30 immunization on the development of early mouse embryos. Methods The CD4 +、CD8 + and CD57 + cells in uterus of SA 30 immunized or control female Kunming mice were detected by immunohistochemical method(LSAB). Results On 3 day of pregnancy, much more CD4 +、CD8 + and CD57 + cells occurred in the uterus of SA 30 immunized mice than those of the control mice. On the other hand, the positive cells were found both in the endometrium and myometrium of immunized mice, but only in myometrium of control mice. Conclusion SA 30 can induce the cell mediated immune responses in mouse uterus, which may be toxical to the early embryos.

Astrocytes are closely associated with Alzheimer's disease (AD). However, their precise roles in AD pathogenesis remain controversial. One of the reasons behind the different results reported by different groups might be that astrocytes were targeted at different stages of disease progression. In this study, by crossing hAPP (human amyloid precursor protein)-J20 mice with a line of GFAP-TK mice, we found that astrocytes were activated specifically at an early stage of AD before the occurrence of amyloid plaques, while microglia were not affected by this crossing. Activation of astrocytes at the age of 3-5 months did not affect the proteolytic processing of hAPP and amyloid plaque loads in the brains of hAPP-J20 mice. Our data suggest that early activation of astrocytes does not affect the deposition of amyloid β in an animal model of AD.
Aldehyde Dehydrogenase ; metabolism ; Alzheimer Disease ; genetics ; metabolism ; pathology ; Amyloid beta-Peptides ; metabolism ; Amyloid beta-Protein Precursor ; genetics ; metabolism ; Animals ; Astrocytes ; metabolism ; Brain ; pathology ; Calcium-Binding Proteins ; metabolism ; Cell Proliferation ; Disease Models, Animal ; Gene Expression Regulation ; genetics ; Glial Fibrillary Acidic Protein ; Glutamine ; metabolism ; Green Fluorescent Proteins ; genetics ; metabolism ; Humans ; Ki-67 Antigen ; metabolism ; Mice ; Mice, Transgenic ; Microfilament Proteins ; metabolism ; Mutation ; genetics ; Nerve Tissue Proteins ; metabolism