目的：观察低剂量辐射（LDR）诱导胸腺细胞凋亡及细胞周期进程适应性反应的基本规律。方法：用X射线照射昆明系雄性小鼠，其诱导剂量（D1）及其后攻击剂量（D2）分别是75 mGy 和1.5 Gy。D1和D2间隔时间分别是3、6、12、24和60 h。D2照射后18 h胸腺细胞培养4、20 和44 h用流式细胞仪检测胸腺细胞凋亡小体（TAB）和细胞周期进程的变化。结果：当D1和D2间隔3、6和12 h，在D2照射后胸腺细胞培养4和20 h，D1 + D2组 TAB 百分数明显低于D2组（P<0.05），G0/G1和G2+M期细胞百分数也不同程度地低于D2组, 而S期细胞百分数却明显高于D2组（P<0.05或P<0.01）。结论：D1和D2分别是75 mGy（剂量率，12.5 mGy/min）和1.5 Gy（剂量率，0.287 Gy/min），D1和D2间隔3～12 h, 在小鼠全身照射后其胸腺细胞培养4和20 h可诱导细胞凋亡和细胞周期进程的适应性反应。

弓形虫急性感染对小鼠雄性生殖机能影响的观察

近年弓形虫感染对男性生殖损害的影响逐渐引起人们关注,但弓形虫感染对雄性生殖机能的影响尚少见.为此,本研究建立小鼠弓形虫感染的动物模型,探讨弓形虫急性感染对雄性生殖机能的影响.

甘草酸软膏治疗豚鼠慢性湿疹模型的实验研究

目的 观察甘草酸软膏抗炎、止痒和对豚鼠慢性湿疹的治疗作用.方法 雄性昆明种小鼠、雌雄昆明种小鼠、白色豚鼠各60只,分别随机分为模型对照组(10只)、基质对照组(10只)、醋酸地塞米松乳膏组(10只)、甘草酸软膏高(10只)、中(10只)、低(10只)剂量组,各组分别建立二甲苯致小鼠耳廓肿胀模型,右旋糖酐40致小鼠搔抓模型,以及2,4-硝基氯苯反复刺激的慢性湿疹豚鼠模型,分别观察甘草酸软膏对小鼠耳廓肿胀和搔抓反应以及慢性湿疹豚鼠耳廓肿胀的影响.结果 甘草酸软膏高、中剂量可以抑制二甲苯致小鼠耳廓肿胀(P＜ 0.05或0.01)；甘草酸软膏高剂量可以延长有旋糖酐致小鼠搔抓的潜伏期,甘草酸软膏高、中、低剂量可减少搔抓次数(P＜ 0.05或0.01),减轻慢性湿疹豚鼠模型耳廓的肿胀(P＜0.05或0.01),并对耳廓皮肤的病理改变有一定的改善作用.结论 甘草酸软膏对慢性湿疹豚鼠模型有一定的治疗作用.

AIM:To examine and compare the effects of several ARBs that are widely used in clinics , on the ACE-Ang II-AT1 receptor and the ACE2-Ang(1-7)-Mas axis during the development of cardiac remodeling after pressure overload .METHODS: All of the mice used in the study underwent transverse aortic constriction (TAC) or sham operation for 2 or 4 weeks.A solution of either ARBs or sa-line was administered through a stomach tube 3 days before the operation .Meanwhile , to eliminate the influence of Ang II , a recombi-nant adenovirus expressing small interfering RNAs targeting angiotensinogen ( Ad-ATG siRNA) was injected via the tail vein .The sur-gery was then performed and the drug was administered as mentioned above .Cardiac function and remodeling were evaluated by echo-cardiography , hemodynamic measurements and cardiac histology .Western blotting was used to determine the protein expression levels . Meanwhile , we performed similar experiments using ARBs with or without ATG siRNA in cardiomyocytes induced by mechanical stretch.RESULTS:Although all of the six ARBs , none of which repressed the elevation of left ventricular pressure after TAC , attenu-ated the development of cardiac hypertrophy and heart failure in the wild-type mice, the degree of attenuation by Olmesartan , Candesar-tan and Losartan tended to be larger than that of the other three drugs tested .Additionally , the degree of downregulation of the ACE-Ang II-AT1 axis and upregulation of the ACE2-Ang(1-7)-Mas axis was higher in response to Olmesartan, Candesartan and Losartan administration in vivo and in vitro.Additionally, Olmesartan had a larger influence when administered long term .However, the expres-sion of ACE was not influenced by the administration of ARBs in vivo and in vitro.Moreover, in angiotensinogen-knockdown mice, TAC-induced cardiac hypertrophy and heart failure were inhibited by Olmesartan , Candesartan and Losartan but not by Telmisartan , Valsartan and Irbesartan administration .Furthermore , only Olmesartan and Candesartan could downregulate the ACE-Ang II-AT1 axis and upregulate the ACE2-Ang(1-7)-Mas axis in vitro.CONCLUSION: Olmesartan, Candesartan and Losartan could effectively in-hibit pressure overload-induced cardiac remodeling even when with knockdown of Ang II , possibly through upregulation of the expres-sion of the ACE2-Ang(1-7)-Mas axis and downregulation of the expression of the ACE-Ang II-AT1 axis.In contrast, Telmisartan, Valsartan and Irbesartan only played a role in the presence of Ang II , and Losartan had no effect in the presence of Ang II in vitro.