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Objective To investigate the effect of long-term high-fat diet on cognitive function and hippocampus neurons ultrastructure in obese rats.Methods Forty SD rats were randomly assigned to a high fat diet (HFD) group and a common diet (CD) group.Meanwhile,HFD-induced obese rat model were established.The spatial learning and memory were measured by the Morris water maze,and the neurons ultrastructural changes in rat hippocampus CA1 region at the corresponding period were observed by transmission electron microscopy.Results The average weight of rats was 25％,28％,and 22％ higher in the HFD group than in the CD group at the 12,16,and 20 weeks,respectively;the Lee's indexes were 6％,4％,and 8％ higher;the average swimming latency were 52％,44％,and 40％ longer;the average swimming distance were 85％,45％,and 51％ longer;the average swimming speed were 57％,34％,and 18％ higher;the duration of staying in the target quadrant were 32％,54％,and 63％ shorter;and the average times of crossing the plate form were 30％,34％,and 34％ shorter,respectively (all P ＜0.001).In comparison of ultrastructure in hippocampus CA1 region of rats at corresponding time points,the amounts of degenerated and necrosis neurons,of the deformed and vacuolar mitochondria,and of the less rough endoplasmic reticulum were significantly more at 12,16,and 20 weeks in the HFD group than in the CD group.Conclusions Long-term HFD-induced obesity damages the structure of neurons in the hippocampus,impairs spatial learning and memory function,and accelerates cognitive aging in rats.
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AIM: To investigate the changes of ultrastructure in early diabetic rat cornea and the pathogenesis of diabetic keratopathy. METHODS: 20 Sprague-Daxley rats were sacrificed 6, 8, 10 and 12 weeks after induction of diabetes mellitus by streptoxotocin. 20 untreated rats at the same age were used as normal controls and were sacrificed at the same intervals. The ultrastructures of cornea were observed with transmission electronic microscopy and scanning electron microscopy. RESULTS: During the experimental period, the corneal ultrustructure of diabetic rats showed that epithelial and endothelial cells were swollen, the mitochondrions in the cytoplasm were swollen and increased. The collagen fibers appeared in disarrangement 10 weeks after streptoxotocin treatment. The endothelial of cornea was damaged from the periphery to the center gradually. CONCLUSION: The ultrastructural changes of cornea leads to dysfunction in streptoxotocin-induced diabetic rats, which may be related to the abnormal metabolism in hyperglycemia condition.
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AIM: To investigate the protective effect of Siduqing, a Chinese medicine, on LPS-induced myocardium injury in mice and its mechanisms. METHODS: Mice were divided into 4 group: control, LPS, Siduqing treatment and Siduqing group, and administered intragastrically with Siduqing decoction or distilled water (0 2 mL/10 g) twice a day for 3 days, two hours after Chinese herbal medicine treatment on day 3, LPS (30 mg/kg) or normal saline was injected intraperitoneally. The serum creatine kinase (CK) and myocardial superoxide dismutase (SOD) activities were determined, and myocardial tumor necrosis factor ? (TNF?) and malondialdehyde (MDA) contents were also detected. In addition, the histological changes and ultrastructure of heart were examined. RESULTS: Histological examination showed edema in myocardium and architectural disarray at 12, 24 h after LPS injection, mitochondrial swelling, condensation and margination of chromatin, irregular nuclear envelope and loss of contractile filaments at 24 h post LPS administration, while Siduqing treatment attenuated the above pathological changes of myocardium. CK activity in serum and myocardial TNF? content were higher in LPS group than control and Siduqing treatment group. Myocardial SOD activity in siduqing treatment group was higher than that in LPS group, but there was no difference in myocardial MDA content between control, LPS and Siduqing treatment group. CONCLUSION: These data suggest that Siduqing protects myocardium against LPS- induced injury via inhibiting myocardial TNF? production.
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AIM: To obverse the expression and localization of urocortin on ultrathin cryosections of syncytiotrophoblast of human term placenta with immunocytochemistry technique under transmission electron microscope. METHODS: The human term placenta tissue from Cesarean delivery and normal labor were fixed in 4% paraformaldehyde, and then divided into two parts. One part was for regular immunocytochemistry under microscope, and the other part was used to prepare ultrathin cryosections for immunocytochemistry under transmission electron microscope. RESULTS: 1.Uroncortin mainly distributed in cytoplasm of syncytiotrophoblast of human term placenta under microscope. Urocortin also appeared in cytoplasm in some stromal cells. 2. Under transmission electron microscope, the anti-urocortin gold particles were observed in cytoplasm of syncytioptrophoblast ultrathin cryosections and sited on rough-surfaced endoplasmic reticulum. The anti-urocortin gold particles also appeared on nucleus and nuclear membrane of syncytiotrophoblast. CONCLUSION: Syncytiotrophoblast of human term placenta synthesized and secreted urocortin. The internalization of urocortin within syncytiotrophoblast nuclear indicates that urocortin may act as intracrine.
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Objective To explore possible mechanisms of hepatic fibrosis by investigating the ultrastructural dynamic changes of liver tissue, especially several kinds of cells related to hepatic fibrosis.. Methods. Murine schistosomal hepatic fibrosis model was established by infecting mice with Schistosoma japonicum cercariae. Routine transmission electron microscopy was used to observe the liver tissue. H.E. staining was used for examining the pathological changes. . Results . H.E. staining showed that the model was established successfully. Ultrastructural observation showed that at the 6th week after infection, the necrosis of hepatocytes around the acute granulomas occurred; the number of sinusoidal endothelial fenestrae and vitamin A droplets in fat-storing cells decreased; large phagosomes and rough endoplasmic reticulum could be seen in the cytoplasm of Kupffer′s cells. At the 8th week, steatosis was found in some hepatocytes, some microvilli emerged on a few inter-hepatocytic surfaces and the inter-hepatocytic spaces were enlarged. Large collagen fibrillar bundles filled in the perisinusoidal spaces, and capillarization of hepatic sinusoids was observed. Secretory vesicles filled with collagen fibrils appeared in the cytoplasm of fat-storing cells with large amount of collagenous fiber bundles surround the cells. Rough endoplasmic reticulum increased in Kupffer′s cells. At the 10th week, fat-storing cells were activated and transformed into myofibroblasts. At the 12th week, the number of myofibroblasts decreased but that of fibroblasts and fiber cells increased. . Conclusion . Activation of fat-storing cells and transformation from fat-storing cells into myofibroblasts are the critical link in the development of hepatic fibrogenesis following schistosome infection. Kupffer′s cells, necrotic hepatocytes and sinusoidal endothelial cells may relate to the activation of fat-storing cells. Capillarization of hepatic sinusoids possibly accelerates the development of hepatic fibrosis.