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@#Background: Auraptene is a simple coumarin that exhibits multiple protective activities in the brain. Alzheimer’s disease is a complex, multifactorial, and progressive neurodegenerative disease. Microinjection of the β-amyloid peptide (Aβ) into the hippocampus of rat has been recognized as a reliable and stable animal model of Alzheimer’s disease, which mimics the memory deficits. In the present study, the memory enhancing effects of auraptene were studied in rats that Aβ was injected into their hippocampus to create a model of Alzheimer’s disease. Methods: Different doses of auraptene (5, 10 and 25 mg/kg) were administered intraperitoneally to male Wistar rats. The spatial memory performance was tested by Morris water maze after Alzheimer`s induction. The hippocampal expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins were calculated for evaluating the neuroprotective and anti-apoptotic effects of Auraptene in the brain tissue. Results: In comparison with the control group, auraptene significantly decreased the escape latency time in the treated rats. In addition, auraptene increased the percentage of time spent and traveled pathway in the target quadrant. Molecular data showed that auraptene attenuated the Bax/Bcl-2 ratio in the hippocampus of rats. Conclusion: This study demonstrated the memory enhancing effect of Aur after Aβ injection, which could be through inhibiting the apoptotic pathways in the hippocampus of rats.
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Objective:To evaluate the effect of sacral nerve stimulation (SNS) for STC by receptor tyrosine kinase c-kit.Methods:Wistar rats were fed with diphenoxylate to make slow transit constipation(STC) rat model.Sacral nerve stimulation(SNS) for the SNS Rat Group.The studied animals were allocated into three experimental groups:STC Rat Group;SNS Rat Group;Normal Rat Group;Every group included 10 rats.The c-kit of ICC in the subserosal layer of rats were analyzed by immunohistochemistry,western blot and RT-PCR.Results:The morphological characteristics of STC Rat Group were not comparable to those of the multipolar c-Kit positive ICC seen in the subserosa of colon of normal rat.In the colon of rat,c-kit protein and c-kit gene in SNS rat group and Normal rat group was significantly higher than STC rat group detecting by western blot.Statistical differences between STC Group and SNS Rat Group were found (P＜0.05);statistical differences between STC Group and Normal Rat Group were also found (P＜0.05).There was not statistical differences between SNS rat group and Normal Rat Group.Conclusion:SNS has effective treatment for the STC rat.
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Background Previous retinal vascular mounting only obtained part of retinal vessels for the study of retinal diseases,and thus it is difficult to comprehensively assess these diseases.So optimizing the trypsin digestion method to show the complete retinal capillary network is very important for the study of retinal diseases.Objective This study was to modify the preparing way of trypsin digested whole retinal capillary network and offer a basis for a quantitative analysis of cells and capillaries.Methods Thirty Wistar rats were divided into model group (20 rats) and control group (10 rats).Streptozotocinum(STZ) of 1.25％ dissolved in 0.05 mmol/L sodium citratehydrochloric acid buffer was intraperitoneally injected to establish diabetes models in the model group,and the equal volume of solvent was used in the same way in the control group.Eight months after injection,100 ml PBS was injected via ventriculus sinister and released via cut right atrium,and then 100 ml 4％ paraformaldehyde was injected into the ventriculus sinister.The rat retinas containing part of the optic nerve were entirely isolated,and digested by trypsin,and vitreous,inner limiting membrane and neural retinal tissue were removed.The whole retinal capillaries network was mounted on the slide.The ghost pericytes and acellular capillaries in the middle retinal area were identified and counted under the optical microscope.Results The retinal mount exhibited that the retinal vessels were stained by hematoxylin and periodic acid schiff.The vessels network presented with the entire type in shape with the radical central retinal arteries and veins and their branches.The capillary showed the shallow-and deep-layer networks between the small arteries and veins.Pericytes distributed and protruded vessel wall and formed the ghost cells without nuclei.The diameter of acellular capillaries was 20％ or more than that of near capillaries,and no cellular nuclei or ghost cell was found through the vessel.Conclusions The experimental technique for setting-up of cleaned vasculature and mounting vessels on glass microscopic slide provides intact vessels,which is helpful for the evaluation of retinal vascular morphology and quantitative analysis.
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Objective: To investigate the effects of Pantoprazole on the expression of TFF1 in stress-induced gastric mucosal lesions in rats, and the mechanism thereof. Methods: Fifty-six rats were randomly divided into seven groups, normal group, model groups (3 groups) and model therapy groups (3 groups). The rat model of water immersion- restraint stress (WRS) was established in model groups, model group1(the immediately after establishing models), model group 2 (4 h after establishing models) and model group 3(8 h after establishing models). The model therapy groups were divided into model therapy group 1 (immediately after establishing models), model therapy group 2 (4 h after establishing models), and model therapy group 3 (8 h after establishing models). The ulcer index (UI) and histological changes were observed after WRS in rats. The expression of TFF1 was detected by immunohistochemistry. Results: After WRS, the gastric mucosa was widely damaged in rats. UI were increased and the expression of TFF1 was decreased in model groups. After intervention with Pantoprazole, UI was lower in model therapy group than those in model groups (model group 1 vs model therapy group 1,69.13±1.97 vs 23.38±1.30, P ＜ 0.01; model group 2 vs model therapy group 2, 57.50±8.81 vs 10.38±3.02, P ＜ 0.01; model group 3 vs model therapy group 3, 43.50±6.76 vs 5.88±1.25, P ＜ 0.01). The staining scores of TFF1 were increased (model group 1 vs model therapy group 1, 0.55±0.11 vs 0.92±O.15, P＜ 0.01; model group 2 vs model therapy group 2, 0.76±0.24 vs 1.36±0.21, P＜ 0.01; model group 3 vs model therapy group 3, 1.12±0.16 vs 1.65±0.11, P ＜ 0.01). Conclusion: TFF1 may participate in the protection of gastric mucosa and promote ulcer recovery. Pantoprazole may participate in the defense of gastric mucosa through mediating the up-regulation of TFFI expression.
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Objective To detect the expression of TrkA in the brain of the Wistar rats during the embryonic phase.Methods Adult Wistar rats were fed in one cage.It was E0 day when sepermia were found in vaginal suppository and vaginal smear.The expressions of TrkA in the brain of Wistar rats during various brain regions were observed by immunohistochemistry on E13,E15,E17,E19 and E21 day. Results On E13 day no obvious expression of TrkA was observed in the embryonic brain.The expression of TrkA had an obviously increasing tendency in the cortex of telencephalon from E15 day to E17 day.And on E17 day,the positive rate of the expression of TrkA reached the second peak.While on E19 day,the expression of TrkA had a temporary decreasing.Then on E21 day the expression of TrkA reached the highest peak.The striatum and hippocampus developed later than the telencephalon till E17 day,and the expressions of TrkA during these stages were same as the cerebrum.Conclusion From E15 to E17 day,obvious expressions of TrkA are observed in the embryonic telencephalon,and it accords with embryonic induction.
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Objective: To study the influence of inflammatory cytokine TNF-? on the expression of adhesion molecules and specific markers of rat MSCs, and to study the optimal stimulation of MSCs with inflammatory factors in inducing adhesion molecule expression which promotes migration of MSCs to the ischemic area in liver. Methods: The MSCs stimulated with different concentration of TNF-? were detected for adhesion molecules and stem cells markers on cell surface with the method of flow-cytometry, MSCs which were stimulated with the optimal concentration of TNF-? and labeled with 1, 1-Dioctadecyl-3, 3, 3, 3-tetramethylindocarbocyanine Iodade(DiI)were delivered intravenously to the rats whose liver was injured by ischemia, the liver function of the experimented animals were tested, and liver samples in the ischemic area were obtained, the number of MSCs was counted under a fluorescent microscope. Results: Stimulated with TNF-?, MSC ex-pression of VCAM-1 increased, while that of stem cell markers did not change markedly. Exposed to lower concentration of TNF-?, the adhesion ability of MSCs obviously increased and more MSCs rested in the ischemic areas in the rat liver, compared to the control groups. Conclusions: TNF-? can increase the expression of VCAM-1 on rat MSCs while exert little effect on the stem cell character of MSCs. Suitable concentration of TNF-? can promote MSCs migration to the damaged tissue, which provides rationale for the treatment of liver disease.
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Objective To study the effects of mild and moderate iodine excess on thyroid function and morphology in Wistar rats with iodine deficiency. Methods Rats with iodine-deficiency were prepared by drinking 1% postassium perchlorate solution followed by drinking double distilled water (DDW) containing 0 ?g/L (iodine deficient control) iodine load, 840 ?g/L or 1680 ?g/L iodine load. Normal rats in DDW group drank DDW with 0 ?g/L iodine and had common diet. Serum TSH was measured with solid phase radioimmunoassay (IRMA) and serum TT_4, TT_3, rT_3 and thyroid TT_4 with radioimmunoassay (RIA). Thyroid morphological changes were observed under optical and electron microscopes. Metamorphic imaging system was used to measure the height of thyrocytes and the area of thyroid follicular cavities. Results At the 90 th day after starting treatment, serum TSH levels in 840 ?g/L iodine group and 1680 ?g/L iodine group were markedly lower than that in iodine-deficient control group (both P
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The effects of different iodide intakes on the thyroid sodium iodide symporter (NIS) mRNA expression, thyroid hormones, urinary iodine and tissue iodine in thyroid were observed. NIS mRNA expression was elevated; and urinary iodine, thyroid tissue iodine and thyroid hormones were significantly lowered in low iodine group. In high iodine group, NIS mRNA expression was inhibited and thyroid hormones decreased. The results show that NIS is the important component of this autoregulatory mechanism. Both low and high iodine intakes can lead to hypothyroidism.