甾体皂苷TSA对局灶性脑缺血大鼠神经发生的影响

目的：探讨甾体皂苷TSA对脑缺血损伤大鼠神经发生的影响。方法：建立大鼠大脑中动脉缺血再灌注模型,随机分为模型对照组,TSA15mg/kg、30mg/kg、60mg/kg剂量组,安宫牛黄400mg/kg阳性对照组以及假手术组。于恢复早期3～14d给药,术后3,7,10,14d观察运动功能的动态变化,免疫组化法检测侧脑室下区brdu阳性细胞数以及梗死周围区巢蛋白的表达。结果：与模型对照组比较,TSA30mg/kg、60mg/kg给药组能够促进脑缺血大鼠横木行走的能力,增加侧脑室brdu阳性细胞数以及Nestin的表达。结论：TSA可改善大鼠脑缺血后神经功能的恢复,可能与其诱导脑缺血后神经发生有关。     

胰腺外分泌功能对肝再生影响的实验研究

目的：探讨胰腺外分泌腺的缺失对残肝再生的影响。方法：采用大鼠亚全胰管结扎（SLPD）模型,在胰腺实质大部分萎缩之后对肝再生和营养状况进行评估。对体重变化率、相对肝重量、肝湿重与体重比以及肝再生率进行计算。结果：SLPD组和SLPD加肝叶切除（Hx)组术后3天体重变化率减轻并呈波动改变,后者体重变化率的恢复缓慢。在单纯SLPD组肝湿重减低而不伴有溴脱氧脲嘧啶核苷（Brdu)标记指数或有丝分裂指数反应的改变。SLPD加Hx组肝再生率低于Hx组,SLPD加Hx组术后第1天残肝Brdu标记指数和有丝分裂指数的峰值明显减低,包括术后第2天有丝分裂指数减低。结论：胰腺外分泌功能对肝细胞的营养和再生有重要作用。     

Inhibition of Cell Proliferation and Induction of Apoptosis During Azoxymethane Induced Colon Carcinogenesis by Black Tea

Tea (Camellia sinensis) is one of the most popular beverages, consumed worldwide. The health promotingproperties of tea have been attributed to its antioxidative polyphenolic constituents and their oxidative products.The aim of the present study was to evaluate the chemopreventive efficacy of a black tea infusion on azoxymethaneinduced colonic preneoplastic lesions, the aberrant crypt foci in Sprague-Dawley rats. Rats were injected withazoxymethane (15mg/kg.b.w.) and received oral administration of 1% and 2% (w/v) tea infusions from the 1st day ofcarcinogen application. The treatment was continued for 12 weeks. The colons were then assessed for aberrant cryptfoci and compared with the untreated carcinogen control group. In situ cell proliferation and in situ apoptosis werealso estimated using Brdu incorporation and the TUNEL method, respectively. Aberrant crypt foci were reducedsignificantly (by 44% in the 1% tea-treated and by about 40% in 2% tea-treated group). Significant decrease inproliferation and increase in apoptosis suggest a possible interplay between the two processes resulting in inhibitionof colon carcinogenesis by black tea.     

Anti-Proliferative and Apoptotic Effects of Etoricoxib,a Selective COX-2 Inhibitor,on 1,2-Dimethylhydrazine Dihydrochloride-Induced Colon Carcinogenesis

In the present study, we assessed effects of etoricoxib, a non steroidal anti-inflammatory drug, on proliferationand apoptosis in 1,2-dimethylhydrazine dihydrochloride (DMH) induced colon lesion development. Male SDrats were divided into four groups: Group 1 controls receiving the vehicle treatment; Group 2 administeredDMH weekly (30 mg/kg body weight, subcutaneously) alone; Group 3, DMH weekly plus etoricoxib (0.64 mg/kgbody weight, orally) daily; and Group 4, etoricoxib alone. After six weeks of treatment, animals were sacrificedand colons were analysed for morphological and histopathological features. Well characterized pre-neoplasticaberrations such as multiple plaque lesions, hyperplasia and dysplasia were found in the DMH treated groupwhereas these features were reduced with co-administration of etoricoxib. To study apoptosis, colonocyteswere isolated by metal chelation from colonic sacs and studied by fluorescent staining and further confirmedby DNA fragmentation. The DMH treated animals had fewer apoptotic nuclei as compared to the controls, butnumbers were higher with DMH+etoricoxib as well as etoricoxib alone. Expression of proliferative cell nuclearantigen (PCNA), assessed by Western blot analysis and immunohistochemistry, was found to be elevated byDMH treatment group and again reduced by etoricoxib. Results for bromodeoxyuridine incorporation (BrdU)were in agreement. It may be concluded that the drug, etoricoxib, has the potential to act as an anti-apoptoticand anti- proliferative agent in the colon.