Influence of chronic intermittent hypoxia on growth associated protein 43 expression in the hippocampus of young rats

This study aimed to explore the pathological change to hippocampal neurons and the expression of growth associated protein 43 in 21-day-old young rats following chronic intermittent hypoxia. Hematoxylin-eosin staining results showed varying degrees of degeneration and necrosis in hippocampal neurons depending on the modeling time. Immunohistochemistry revealed that growth associated protein 43 expression in young rats following chronic intermittent hypoxia decreased, but that levels were still higher than those of normal rats at each time point, especially 4 weeks after modeling. During 1 5 weeks after modeling, a slow growth in rat weight was observed. Experimental findings indicate that chronic intermittent hypoxia may induce growth dysfunction and necrosis of hippocampal neurons, as well as increase the expression of growth associated protein 43 in young rats.

MORPHOLOGICAL STUDY OF FETAL NEOCORTICAL TRANSPLANT GRAFTED TO THE CEREBRAL CORRESPONDING AREA IN YOUNG RATS DIFFERENTIATION OF IMMATURE NEURONS AND RECIPROCAL CONNECTIONS OF FIBERS BETWEEN GRAFT-HOST BRAIN

The fetal neocortical transplant (E15-17 days gestation) of Wistar rat was grafted to the corresponding neocortical region (frontal-parietal lobe) of the same strain in young rats (4-5 weeks old). On the 7th, 15th, 30th, 60th, 150th day after transplantation, the sections cut through the middle area of graft-ost brain were examined by HE, Nissl, Glees stain, immunohistochemical technique for GFAP and NF, Nissl, Glees stain, immunohistochemical technique for GFAP and NF, acetylcholinesterase (AChE) histochemistry as well as horseradish peroxidase (HRP) retrograde tracing with light microscope. Some of the sections were also examined with TEM. The result showed that most immature neurons within the graft can survive, grow, differentiate and mature, and are similar to the structure of the neocortical neurons of host brain. This study also provides patterns of integration of the interface between graft-host brain varying with the proliferation of reactive astrocyte as well as graft-host reciprocal connection of fibers.

Effect of Huanglian Jiedu Decoction on vascular endothelium factor and expression of RhoA protein factor in young spontaneously hypertensive rats

To investigate the mechanism of effect of Huanglian Jiedu Decoction(HLJD) on vascular endothelium, we assessed the protective effect of HLJD on vascular endothelium in spontaneously hypertensive rats(SHR) and the expression of RhoA in thoracic aorta. A total of 40 SHR rats were randomly and evenly divided into model group(SHR group), positive group(captopril group), HLJD high-dose group, and HLJD low-dose group. Simultaneously, 10 Wistar Kyoto rats were used in the blank group. All groups were treated by gavage for 6 weeks. The changes of nitric oxide synthase(NOS), von Willebrand factor(vWF), endothelin(ET-1) and calmodulin(CAM) in rat serum were tested by enzyme linked immunosorbent assay(ELISA) method. The expression of RhoA at the protein and mRNA levels in thoracic aorta was determined by Western blotting(WB) and quantitative real-time PCR, respectively. Compare with the blank group after 6 weeks, the levels of ET-l and VWF in serum of the model group were significantly increased(P<0.01), and the levels of NOS and CAM were significantly decreased(P<0.01). Conversely, the levels of ET-1 and vWF in the positive and HLJD groups were significantly decreased(P<0.01 or P<0.05), and the levels of NOS and CAM were significantly increased(P<0.01 or P<0.05) compared with the model group. The expression of Rho A at the mRNA and protein levels was decreased obviously(P<0.05) in HLJD high-dose group. The results shown that HLJD increased diastolic factor(CAM and NOS) in the vascular endothelial of rats, leading to reduced contraction factor(ET-1 and vWF). HLJD revealed the preventive function in the vascular endothelial dysfunction of the early stage hypertension through adjusting secretion of blood vessel endothelium(BVE) relaxing factor and improving vascular endothelial function. The mechanism might be associated with the inhibition of the activity of RhoA protein factor.