右美托咪定抑制NOX4缓解急性应激致大鼠肾损伤

本研究拟探索右美托咪定（dexmedetomidine,DEX）对大鼠急性应激致肾损伤的保护作用,并从氧化应激的角度探索DEX对大鼠肾的保护通路。本研究使用了急性束缚应激模型,其中,大鼠被迫游泳15 min,并束缚3 h。本试验采用生化检测、组织病理学切片观察以评估肾功能,然后测定了氧化应激以及氧化应激的相关通路蛋白。旷场试验证实成功建立了急性应激模型。急性应激引起的肾损伤增加了NOX4,降低了Nrf2/HO-1/NQO1表达水平。DEX可降低NOX4表达,同时升高Nrf2/HO-1/NQO1的表达水平。DEX治疗组与急性应激组相比的肾生化结果明显恢复正常,病理切片观察损伤显著降低。试验结果表明,DEX治疗急性应激可影响NOX4/Nrf2/HO-1/NQO1信号通路,并抑制氧化应激。因此,DEX对急性应激引起的肾损伤具有保护作用,并在应激综合征中具有潜在的临床应用。     

对汽车撞柱的仿真研究

由于许多汽车事故是因为车辆撞枉而造成的，根据采集得到的真实事故数据，应用LS—DYNA和MADY—MO对车辆撞柱进行仿真，时仿真结果与事故调查结果比较分析表明，该仿真结果能真实反应实际撞柱情况，仿真方法的有效性得以证实。     

Effects of naringenin on PI3K/AKT signaling pathway and endoplasmic reticulum stress and its related apoptotic pathways in rats with myocardial ischemia/reperfusion injury

AIM To observe the effect of naringenin on cardiac injury in ischemia/reperfusion （I/R） rats, and to explore whether the role of naringenin is involved in PI3K/AKT signaling pathway and endoplasmic reticulum stress and its related apoptotic pathways. METHODS SD rats （n=48） were randomly divided into sham operation （sham） group, model （I/R） group, naringenin treatment （NAR） group and naringenin+LY294002 （NL） group. Myocardial I/R injury model was prepared by ligation of left anterior descending coronary artery of rats for 30 min followed by reperfusion for 120 min. After reperfusion, the serum levels of cardiac troponin I （cTnI） was measured by ELISA. HE staining, TTC staining and TUNEL staining were used to detect the myocardial histopathological changes, myocardial infarction area and myocardial cell apoptotic rate. The mRNA levels of endoplasmic reticulum stress-related indicators glucose-regulated protein 78 （GRP78）, C/EBP homologous protein （CHOP） and caspase-12 were detected by RT-qPCR. The protein levels of cleaved caspase-3, GRP78, CHOP, caspase-12, p-PI3K and p-AKT were determined by Western blot. RESULTS Compared with I/R group, the serum content of cTnI, myocardial pathological damage, myocardial infarction area and myocardial cell apoptotic rate were significantly reduced （P<0.05）, the protein levels of cleaved caspase-3, GRP78, CHOP and caspase-12 were decreased （P<0.05）, and the protein levels of p-PI3K and p-AKT were increased in NAR group （P<0.05）. LY294002 attenuated the protective effect of naringenin to some extent. CONCLUSION Naringenin reduces myocardial I/R injury in rats possibly by activating PI3K/AKT signaling pathway and subsequently regulating endoplasmic reticulum stress and its related apoptotic pathways.     

敌草快对斑马鱼组织损伤及慢性肝脏损害作用

探讨敌草快对斑马鱼(Brachydanio rerio)的毒性效应及其致毒机理。观察敌草快对斑马鱼鳃和肝脏组织的急性损伤效应,并分析慢性敌草快胁迫对斑马鱼肝脏超氧化物歧化酶(SOD)、谷胱甘肽-S转移酶(GST)、丙二醛(MDA)和甘油三酯(TG)的影响。敌草快对斑马鱼的96 h半致死浓度(LC50)为16.92 mg·L~(-1);斑马鱼暴露于8.46、4.23、1.69 mg·L~(-1)敌草快中96 h后,苏木精-伊红(H-E)染色显示鳃小片出现卷曲变形、上皮细胞排列不规则和细胞脱落现象,肝细胞呈现明显的肿大,胞质产生空泡化,局部区域细胞坏死、溶解,斑马鱼鳃和肝脏组织的损伤程度随着敌草快浓度的增加而加重;暴露于1.69、0.84 mg·L~(-1)和0.34 mg·L~(-1)敌草快中28 d后,斑马鱼肝脏的SOD活性变化表现为降-升-降,并呈现出剂量效应;1.69 mg·L~(-1)和0.84 mg·L~(-1)敌草快处理组肝脏的GST活性表现为先升后降,28 d时显著低于对照组(P0.01),0.34 mg·L~(-1)敌草快处理组肝脏的GST活性无显著变化(P0.05);与对照组相比,处理组肝脏的MDA含量在第7 d和14 d变化均不明显(P0.05),在第28 d时0.84 mg·L~(-1)和1.69 mg·L~(-1)敌草快处理组肝脏的MDA含量极显著升高(P0.01);处理组斑马鱼肝脏中TG的含量均从14 d开始出现增加。水体中的敌草快对斑马鱼有较严重的急性损伤作用,长时间暴露于低浓度敌草快中的斑马鱼,其肝脏会发生氧化应激反应,肝脏代谢功能也会受到影响。     

高海拔地区反季节辣椒烟青虫无公害防治技术

2005年在贵州省毕节市梨树镇平乡村对烟青虫(Helicoverpa assulta Guenée)危害辣椒发生情况调查及采用5种农药进行无公害防治试验,筛选出3种防效较高的农药.防治效果分别达88.03%～94.29%,85.97%～93.88%和82.94%～94.29%.