Effects of Sini decoction on the ultrastructure of small intestinal epithelial cells in rats with intestinal ischemia-reperfusion

AIM: To investigate the effect of Sini decoction (SND)on the ultrastructure of small intestinal epithelial cells in rats with intestinal ischemia-reperfusion. METHODS: Thirty-two Sprague-Dawley rats of both sexes were randomly divided into 4 groups: (1) Control group in which sham operation was performed; (2) Model group in which intestinal I/R was produced by clamping super mesenteric artery(SMA) for 1 hour and declamping SMA for 3 hours; (3) SND1 group in which SD (0.6 g/200 g rat) was given via stomach tube 3 d before intestinal I/R; (4) SND2 group in which SD (1.2 g/200 g rat)was given via stomach tube 3 d before intestinal I/R. A strip of small intestine was taken from distal end of ileum for electron microscopic examination. The two-dimensional structural parameters and three-dimensional structural parameters of mitochondria were calculated. RESULTS: (1)Morphological changes of small intestine: In control group, epithelial cells were orderly arranged, with normal mitochondria and intestinal villi. In model group, the gaps between epithelial cells widened. There were a lot of apoptotic cells. Microvilli were short and swelled. Mitochondria were swelled obviously with broken ridges. Endoplasmatic reticulum was severely dilated. In SND1 and SND2 groups, microvilli and epithelial cells were orderly arranged relatively, mitochondria was slightly swelled. (2) Structural parameters of mitochondria: In model group, there were the least mitochondria and the swelling of mitochondria was severe. In SND1 and SND2 groups, the mitochondria was more than that of model group and the swelling were slight. CONCLUSION: Sini decoction can protect small intestine from ischemia-reperfusion injury without dose-dependent effect.     

龙眼寒冻害研究进展

从影响龙眼冻害因素、冻害分级、抗冻机理及龙眼冻害前后的管理措施等方面对龙眼抗冻进行了较全面的总结和归纳,为深入探讨龙眼抗冻性机理提供了理论依据.     

渗透胁迫诱导水稻幼苗的氧化伤害

水稻幼苗在渗透胁迫下，随着胁迫强度的增加及时间的延长，O2和H2O2大量产生，膜脂过氧化加剧，细胞膜的完整性受到破坏，离子大量外泄；严重渗透胁迫亦使叶绿素——蛋白质复合体结合松弛，叶绿素含量明显降低。活性氧清除剂α-生育酚、抗坏血酸及甘露醇可阴抑渗透胁迫所诱导的丙二醛增生，减少叶绿素的氧化破坏。这些结果表     

人体颈部动力学响应分析有限元模型的建立和验证

根据汽车碰撞事故中人体颈部损伤防护技术研究的需要。建立了一个人体颈部三维有限元模型。该模型参照人体解剖结构模拟了颈椎骨、椎间盘、小关节、韧带、肌肉和软骨等组织，共由15811个单元构成。各组织的材料特性采用了弹性、粘弹性、和刚性材料模型来描述．模型用前碰撞志愿者实验数据进行了验证。其头部的加速度、位移曲线与实验数据得到了较好的吻合。本文初步研究了软组织特性参数对于颈部运动的影响。该模型具有较高的生物逼真度，可对头颈部在汽车碰撞载荷条件下的加速度、速度、位移等动力学响应参数进行分析研究。     

车前子提取物抑制扑热息痛诱导小鼠肝损伤的作用研究

【目的】研究车前子提取物干预扑热息痛(Acetaminophen,APAP)引起小鼠肝损伤的作用,并探究其潜在作用机制。【方法】运用半仿生酶法提取车前子活性成分,采用液相色谱-质谱联用(LC-MS)检测其主要成分。体内研究车前子提取物对APAP肝损伤的保护作用,将60只雌性昆明小白鼠随机分为正常对照组(NC)、APAP肝损伤模型组(LD)、车前子对照组(PA)以及APAP干预的车前子提取物高、中、低剂量组(HPA+LC、MPA+LD、LPA+LD)。其中NC组和LD组小鼠灌胃生理盐水、PA组小鼠灌胃200μg/mL车前子提取物,HPA+LD,MPA+LD和LPA+LD组小鼠分别灌胃车前子提取物200,100,50μg/mL,每天2次,连续6 d;末次给药12 h后,采血并分离肝脏,检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST)活性,评价肝脏损伤程度;检测肝脏中超氧化物歧化酶(SOD)活性及谷胱甘肽(GSH)、过氧化氢(H_2O_2)和丙二醛(MDA)含量,评价肝脏的氧化应激程度;检测CYP2E1 mRNA和蛋白表达,并通过细胞色素P450酶2E1(Cytochrome 2E1,CYP2E1)法体外筛选车前子抗APAP肝损伤可能的有效成分。【结果】LC-MS检测发现,车前子提取物有37种主要成分;血清生化指标检测发现,不同剂量的车前子提取物明显减少APAP诱导的氧化产物,增强抗氧化防御能力,减轻肝脏损伤且呈剂量依赖性;车前子提取物显著降低CYP2E1 mRNA和蛋白表达,说明车前子抑制CYP2E1的活性;车前子提取物中抗APAP肝损伤的有效成分为车前草苷D、车前草苷E、高车前素和高车前苷。【结论】车前子提取物的有效成分为车前草苷D、车前草苷E、高车前素和高车前苷。车前子提取物对APAP诱导的肝损伤具有保护作用,其潜在作用机制可能与抑制肝脏CYP2E1的表达和活性有关。     

小麦抗寒性机理研究

根据小麦生长规律,许多品种在发育过程中需要一定时间和强度的低温,但极端的温度对产量构成因素的协调提高有不利影响,这种反应是遗传决定的,如小麦的抗寒性。冬季的严酷条件可以减少单位面积内植株数目和降低存活植株的生活力从而对第一个产量构成因素产生不利的影响。有效分蘖力高的品种可以部分地或全部地弥补冬季的损失。可是人们的目的在于使秋季生长的植株全部能够存活下来,这样能形成较多主穗从而对第二和第三个产量构成因素有利。就小麦品种抗寒性、冻害产生的机理进行了论述,以期对培育出的小麦新品系进行抗寒性评价,并对选育该类小麦品种的方法进行探讨。     

基于二次正交旋转组合设计的西葫芦果实 贮前热处理条件的优化

为明确热水处理减轻西葫芦果实冷害的最佳处理条件,以“绿丰”西葫芦为材料,电解质外渗率y为冷害的表征指标,在单因素试验基础上,采用二次正交旋转组合试验设计,研究热处理温度x₁、热处理时间x₂对西葫芦果实表征函数影响,并经统计分析,建立数学模型。 结果表明,所得回归方程为y= 142.608 647-0.690 821x₂ + 0.051 444 x₁² + 0.007 499 x₂²,达到极显著水平,且无失拟因素存在;在热处理（43.3℃、28.4 min）的最佳工艺条件下,于（4±0.5）℃低温下胁迫10 d后西葫芦果实电解质外渗率实测值为33.41%,与理论值相对误差为0.95%,较未处理组降低了27.26%。该试验优化西葫芦果实冷害减轻的热处理工艺参数准确可靠、稳定、可行,为西葫芦采后贮藏技术与果蔬冷害防治的进一步研究提供了一定的技术依据。     

Ozone sensitivity of Phaseolus vulgaris in relation to cultivar differences,growth stage and growing conditions

Exposure of Phaseolus vulgaris cv. Lit to ambient ozone caused a 14% pod yield reduction in 1994. This yield loss was assessed by comparing plants that were protected against ozone by treatment with EDU (ethylenediurea) with unprotected plants, both cultivated in pots with a continuous water supply. The plants had experienced an AOT40 of 8135 ppb.h during their growth. However, plant response to ozone depends on a large number of environmental and plant-specific conditions. Visible injury increased mainly after flowering and was much less severe on soil-grown bean cultivars (Lit, Stella and Groffy) not receiving additional water. Ozone fumigations in closed chambers before or after flowering proved that the growth stage during which the plants are exposed also plays a very important role with regard to injury development. Plants seem to be more susceptible during the generative growth stage and the relative cultivar sensitivity was related to the developmental stage during fumigation. However with regard to yield effects the timing of the ozone exposure seems to be less important.     

ZD制剂对马肢蹄软组织损伤部位肌组织形态及VEGF和bFGF表达的影响

ZD制剂为治疗马非开放性软组织损伤的经典验方,为探索其作用机制,通过建立马前肢急性软组织损伤模型,对其进行组织形态学观察,评价ZD制剂对马急性软组织损伤的作用效果,采用免疫组织化学方法检测ZD制剂对VEGF、bFGF在肌肉中表达的影响。用20匹蒙古马随机分为4组,选取左前肢肩部臂部肌肉,制造急性软组织损伤模型。于造模前、后用取样器进行组织取样,制作成石蜡切片,观察其形态学变化,用免疫组织化学方法对阳性细胞分析VEGF、bFGF的表达。结果表明,试验药物组在损伤后的修复能力优于阳性药物组和阴性对照组。表明ZD制剂可通过促进成纤维细胞、毛细血管新生和肌细胞的生成来进行组织的修复再生,试验药物组在损伤后VEGF、bFGF的表达优于阴性对照组和阳性药物组,ZD制剂可能通过提高VEGF、bFGF的表达进行损伤的修复。     

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.