目的：探讨淀粉样β蛋白42（Aβ42）在正常大鼠视网膜节细胞中的发育及表达。方法：SD大鼠分为正常见光组和避光饲养组。眼球做冷冻切片和视网膜裱片，采用免疫细胞化学方法检测Aβ42的表达。结果：出生后3、6、13d组大鼠视网膜节细胞未见Aβ42表达，15d（见光后）以后开始有表达,并逐渐增多，90d 组表达最多。其中15d和25d组在避光饲养下未见表达。结论：Aβ42在正常大鼠出生后第15日开始表达，并逐渐上调；在15d后避光饲养动物的视网膜节细胞中未见表达，提示该蛋白在视网膜视觉功能的发育中可能发挥了重要作用。

目的：观察毛葡萄叶水提物对FeCl3诱导大鼠血栓形成的影响及主要作用机制。方法：预防性给药10天后用FeCl3诱导大鼠颈总动脉血栓形成模型观察血栓形成,测定血栓湿重, HE染色观察血栓的形态学变化；放射免疫法测定血栓素(TXB2) 、前列环素（62keto2PGF1α) 、内皮素（ET）变化,探讨其作用机理。结果：毛葡萄叶水提物对FeCl3诱导大鼠血栓湿重明显减轻;血浆TXB2、ET降低, 62keto2PGF1α水平升高。结论：毛葡萄叶水提物有明显抗血栓形成作用，其机制与血管ET及血液TXB2和62keto2PGF1α含量水平有关。

为更好地研究血管平滑肌细胞增生性疾病的机理及防治，建立一种体外VSMC增殖器官模型,并对其机制作初步探讨。HE染色和免疫组化染色显示,大鼠主动脉段在体外拉伤内皮并经20 %血清培养后,会出现中膜VSMCs 的增殖。体外培养5 d 后血管壁VSMC就出现不同程度增生，其中13 d 的血管有明显斑块形成；免疫组织化学染色见有标记的增生VSMCs；RT2PCR 检测显示，Hrg21和SM22αmRNA 的表达随培养天数增多而减少，至13 d 检测不出。而在同样体外培养10d情况下，与对照组相比内皮损伤组培养上清中ET21 明显增多，Hrg21、SM22a mRNA 表达下调，Brdu标记增殖细胞增多，当加入内皮素受体阻断剂BQ123后标记细胞明显减少，其中血清培养组与无血清培养组相比，以上检测变化有显著性差异。结果表明，大鼠主动脉经体外培养能诱导平滑肌细胞异常增生并且表型从收缩型向合成型转化，ET21 和血清作用是该模型平滑肌增殖的主要因素。本模型为研究血管平滑肌增殖性疾病的机理和防治提供了一个较好的实验平台。

Development of a cultured tissue experimental model of rat aorta was explored in order to study mechanism of vascular smooth muscle (VSMC) proliferation. This particular model has potential with regard to amelioration of atherosclerosis and other vascular diseases in comparison to whole animal and cell culture models. The aorta segments of rats were divided into 4 experimental groups: the injured endothelium, injured endothelium plus BQ123, without injured endothelium and without injured endothelium plus BQ123. Each of group was subdivided into a further 2 subgroups and cultured with 20% serum and with serum-free DMEM. Each group cultured in vitro for 5, 8 and 13 days respectively. The control group was not cultured in vitro. Bromodeoxyuridine (BrDU 8×10−4 mol/l) was added into the cultured medium of all groups, 24 h prior to harvesting. These segments were fixed in 4% paraformaldehyde for paraffin slice used to HE and immunocytochemical staining and other aorta segments were used to detect the expressions of hypertension-related gene-1 (HRG-1) and smooth muscle 22 alpha (SM22α) by RT-PCR. ET-1 content in the supernatant was detected with radioimmunology. Proliferous VSMC can be observed on artery segments cultured in vitro, and conspicuous plaques were developed on model vascular wall cultured for 13 days. Labeled cells increased with an increase in culture time but were not seen in the control group. Agreater number of labeled cells were observed in injured endothelium group cultured in 20% serum DMEM. Hyperplasia was inhibited after BQ123 was added into the medium, suggesting that serum and ET-1 are important factors that lead to VSMC proliferation. Expressions of HRG-1 and SM22α were decreased while the aorta segments were cultured in vitro, minimum or even absent mRNA expressions of HRG-1 and SM22α were detected in injured endothelium cultured in 20% serumDMEMand increased in injured endothelium plus BQ123 group cultured. ET-1 content in the supernatant increased in injured endothelium cultured in 20% serum DMEM. These results show that the phenotypic transform and VSMC proliferation on cultured artery segments were related not only to serum culture, but also to ET-1 secreting. ET-1 and serum may be the main factors of contributing to the proliferation and phenotypic transform. This model provides a favorable experimental platform for research into the mechanism of vascular proliferous diseases as well as its prevention and treatment.

Objective: To investigate the effect of norepinephrine (NE) on the proliferation and phenotypic transformation of vascular smooth muscle cells (VSMCs) and the mechanisms underlying this effect. Methods: VSMCs were isolated from the rat abdominal aorta. VSMCs cultured in both serum-containing or in a serum-free medium were treated with NE, oxidized low-density lipoprotein (ox-LDL), α-adrenergic receptor agonist (α1-R−), β1-adrenergic receptor antagonist (β1-R−) and various combinations of these factors. VSMC proliferation was determined by bromodeoxyuridine (BrdU) assays. The mRNA expression level of HRG-1 and SM22α were determined by reverse transcription-polymerase chain reaction (RT-PCR). Results: The expressions of HRG-1 and SM22α mRNA in NE-or OX-LDL-treated VSMCs was down-regulated, and the proliferation of BrdU-labeled cells increased; the expression of the abovementioned genes in the VSMCs treated with a combination of NE, α1-R, and β1-R was significantly up-regulated. However, NE was observed to up-regulate the expression of HRG-1 and SM22α mRNA in serum-starved VSMCs. Conclusion: NE could reversibly regulate the proliferation and phenotypic transformation of VSMCs. This regulation might be mediated via its receptors.