热应激对小鼠精液品质的影响及其在全球变暖背景下的生态意义

为了研究全球变暖和局部极端高温气候对雄性小型啮齿类动物繁殖能力的影响,建立小鼠热应激模型,设立5个温度组28、31、34、37和40℃,其中28℃组为对照组。在14d内分别在第1天—第3天、第5天、第7在、第10天和第14天检测小鼠的精子活力、精子顶体完整率、精子畸形率。结果显示,温度越高,精液质量下降越快;温度在较温和的范围内变动时,精液质量随温度的升高而呈现下降的趋势,但经过一段时间的适应,有所回升;在极端温度(40℃)胁迫下,小鼠的精液质量持续下降而不能得到恢复。这说明,高温影响下,雄鼠的繁殖能力存在适应性生理调节过程,但影响是相当明显的,至少在短期内不能恢复到原来水平。由此可以推断,自然界中,较长的精液品质下降期和恢复期可能打破了与雌鼠发情周期的同步化(如果高温对雌鼠影响不大),在自然界中可能对雌鼠的受孕率产生明显影响。此外,即使雌鼠能在雄鼠精液品质恢复期之前受孕,精子损伤也会明显降低受孕率,还可能产生活力低下、畸形或存在其他生理缺陷的后代,进而影响成活率。     

速效救心丸与复方丹参片对孕鼠血液的影响

为了观察速效救心丸、复方丹参片对妊娠小白鼠宫内发育迟缓血液指标的影响.将60只雌鼠随机分为对照组、速效救心丸组和复方丹参片组.对照组给予基础日粮,速效救心丸组用剂量为500mg·kg-1速效救心丸拌饲,复方丹参片组用剂量为500mg·kg-1复方丹参片拌饲.妊娠15d时颈静脉采血, CA-500全自动血液分析仪分析样品.结果表明,与对照组比较,速效救心丸组RBC、WBC、LYM、MON显著升高(P＜0.05),复方丹参片组MON显著升高(P＜0.05),WBC、LYM极显著升高(P＜0.001).说明速效救心丸、复方丹参片对妊娠小白鼠血液细胞有明显升高作用,可在缓解妊娠母鼠IUGR上具有一定的作用.     

大红袍茶降血糖作用研究

[目的]探讨大红袍茶的降血糖作用。[方法]取50只小鼠以200 mg/kg剂量、间日2次腹腔注射四氧嘧啶制造高血糖模型,4 d后得到24只血糖高于9.00 mmol/L的高血糖模型小鼠。将高血糖小鼠按相似血糖水平分为对照组和试验组,血糖值分别为（15.11±6.47）和（14.77±5.40）mmol/L,组间无显著差异（P〉0.05）。对照组饲喂基础饲料和凉开水,试验组在基础饲料中添加3.0%的大红袍茶,饮0.5%的大红袍茶汤。饲养7 d后再次测定血糖值,研究其变化。[结果]对照组小鼠血糖值为（12.23±5.11）mmol/L,无显著变化（P〉0.05）;试验组小鼠血糖值下降到（7.93±1.88）mmol/L,降低了46.3%,变化极显著（P〈0.001）。[结论]大红袍茶对高血糖小鼠有极显著的降糖作用。     

复方桑黄口服液粗多糖对小鼠免疫功能的影响

研究复方桑黄口服液粗多糖对小鼠免疫功能的影响。从小鼠碳廓清实验、小鼠腹腔巨噬细胞吞噬鸡红细胞实验（半体内法）、脏器与体重比值、小鼠自然杀伤（ NK）细胞活性测定（乳酸脱氢酶测定法）等四个方面进行研究。结果表明：复方桑黄口服液的高剂量组（40 ml/kg）能明显增强小鼠碳廓清能力,中（20 ml/kg）、高剂量组能明显增强小鼠巨噬细胞吞噬鸡红细胞的吞噬百分率和吞噬指数,低（10 ml/kg）、中、高剂量组能明显增强小鼠 NK细胞活力功能。这表明复方桑黄口服液具有增强单核-巨噬细胞功能、增强 NK细胞活力功能,复方桑黄口服液具有增强免疫功能的作用,可显著提高机体特异性和非特异性免疫功能。     

不同剂量阿苯达唑治疗鼠旋毛虫病效果初探

使用不同剂量阿苯达唑对人工感染旋毛虫的小白鼠进行疗效试验,观察其不同剂量的杀虫效果.结果表明：应用阿苯达唑20 mg/（kg·d）×7治疗鼠旋毛虫病有很好的治疗效果,为阿苯达唑临床应用提供科学参考.     

Butylated hydroxyanisole promotes expression of neural specific genes in mouse fetal liver cells through extracellular signal-regulated kinase signaling pathways

AIM: To study the mechanism of butylated hydroxyanisole-induced neural differentiation of fetal liver Sca-1+ cells in vitro. METHODS: Sca-1+ cells from 14.5-day-old mouse fetal liver were isolated with a magnetic cell sorting kit. Cultured cells pretreated with or without extracellular signal-regulated kinase (MEK1) inhibitor, PD98059, were induced by 200 μmol/L butylated hydroxyanisole (BHA) for 24 hours, and then incubated in serum-free medium. Expression of genes in treated or untreated cells were assayed by Western blotting and RT-PCR. RESULTS: There was low level of neuronfilament-L (NF-L) and brain factor-1 (BF-1) in fetal liver Sca-1+ cells, but no neuronfilament-H (NF-H) and tyrosine hydroxylase (TH) was observed. BHA significantly promoted the expression of neuron-specific NF-L, NF-H, BF-1, and TH in fetal liver Sca-1+ cells. NF-L, NF-H, BF-1 and TH increased by 6.32 fold, 2.73 fold, 3.37 fold and 2.68 fold, respectively (all P<0.01 vs untreated cells). However, the expression of BHA-induced genes were inhibited by ERK kinase inhibitor PD98059 (25 μmol/L). CONCLUSION: BHA induces neural differentiation of fetal liver cells through ERK.     

Effects of sodium fluoride on hepatic toxicity in adult mice and their suckling pups

In this investigation, we have evaluated the effect of sodium fluoride (NaF) on hepatic function in pregnant and lactating mice and their suckling pups. Experiments were carried out on female Wistar mice given 500 ppm sodium fluoride (226 ppm fluoride ion) in their drinking water from the 15th day of pregnancy until day 14 after delivery. All mice were sacrificed on day 14 after parturition. Our results showed a significant decrease in serum levels of total protein and albumin, a marked hypoglycaemia and a significant decline in serum cholesterol and triglyceride levels in fluoride-treated mice and their pups. Whereas globulin and biluribin levels in serum were not significantly changed by NaF treatment. On the other hand, serum transaminase activities (aspartate transaminase; alanine transaminase), which well known as markers of liver function, were elevated indicating hepatic cells’ damage after treatment with fluoride. Lipid peroxidation increased in NaF-treated mice and pups, as revealed by high liver malondialdehyde levels, while serum total antioxidant status showed a significant decline. These biochemical modifications in NaF-treated mice also correspond histologically with extensive ballooning, hepatocellular necrosis and infiltration of mononuclear cells. These effects were not observed in controls.     

Effect of uric acid on the maturation and the biological function of BMDCs

AIM: To investigate the effect of uric acid on the maturation and the biological function of murine bone-marrow derived dendritic cells (BMDCs) in vitro.METHODS: BMDCs were cultured with GM-CSF, IL-4, LPS and uric acid. Cell phenotypes were analyzed by flow cytometry. MTT was used to detect the effect of uric acid on the function of BMDCs in stimulating the proliferation of T cells. IL-12 released by BMDCs was also detected. RESULTS: BMDCs were cultured and identified. Uric acid at concentrations of 200 mg/L and 400 mg/L increased the expression of the molecules (CD11c, CD83, CD86, IA/IE) on BMDCs surface and the IL-12 level in the culture supernatants (P<0.05), promoted the proliferation of T cells at the T: DC rate 5∶1, 10∶1, 20∶1 (P<0.05). However, uric acid at concentration of 70 mg/L had no effect on above molecule expression (P>0.05), no effect on T cell proliferation with BMDCs (P>0.05) was observed. CONCLUSION: Uric acid promotes the differentiation, maturation, the expression of co-stimulatory molecules, the IL-12 production in BMDCs and enhances the ability of BMDCs to stimulate the proliferation of T cell in a specical dose range.     

The anticancer activity of genistein on implanted tumor of human primary gastric carcinoma cells in nude mice

AIM: To investigate the apoptosis of implanted tumor of primary human gastric cancer cells in nude mice induced by genistein and the relation between this apoptosis and expression of bcl-2 and bax.METHODS: Establishing a transplanted tumor model by injecting human primary gastric cancer cells into subcutaneous tissue of nude mice.The different doses of genistein (0.5mg/kg,1mg/kg and 1.5 mg/kg ) were directly injected beside tumor body respectively,for six times at an interval of two days.Then changes of tumor volume were measured continuously and tumor inhibition rate of each group was calculated.We observed the morphologic alteration by electron microscope,measured the apoptotic rate by TUNEL staining method,detected the expression of apoptosis-regulated gene bcl-2 and bax by immunohistochemical staining and RT-PCR.RESULTS: Genistein could significantly inhibit carcinoma growth when it was injected near the carcinoma.Genistein induced implanted tumors cells to undergo apoptosis with apoptotic characteristics by transmission electron microscope.The apoptosis index of above three groups was increased progressively.Positive rate of Bcl-2 protein of above three groups was decreased progressively and positive rate of Bax protein of above three groups was increased progressively by immunohistochemical staining.The density of bcl-2 mRNA decreased progressively and the density of bax mRNA increased progressively with elongation of time by RT-PCR.CONCLUSION: Genistein is able to induce the apoptosis of transplanted tumor cells.This apoptosis may be mediated by down-regulating bcl-2 and up-regulating bax mRNA and its protein.     

Mechanisms for protection of berberine against LPS-induced acute lung injury in mice

AIM:To investigate the mechanisms by which berberine attenuates LPS-induced acute lung injury, and provide a new strategy for the treatment of the lung injury due to LPS. METHODS:BALB/c mice were randomly assigned into three groups (control, LPS group, and berberine treatment group). Mice were administered intragastrically with distilled water (0.1 mL/10 g) or neutral sulfate berberine (50 mg/kg) once a day for 3 days, 1 h after intragastrical treatment on day 3, LPS (20 mg/kg) or normal saline was injected intraperitoneally (ip). All animals were sacrificed 12 h after LPS injection, the left lung tissue sections were prepared for histology analysis and the right lung were used to determine the ratio of wet to dry lung tissue weight (W/D). In another experiment, bronchoalveolar lavage fluid (BALF) was collected, and then the total protein content, and the amounts of white blood cells (WBC) and polymorphonuclear neutrophils (PMN) in BALF were determined. Furthermore, the phosphorylation of cytosolic phospholipase A₂ (cPLA₂) was detected with immunohistochemical analysis by using phospho-cPLA2(Ser505) antibody, and the contents of thromboxane B₂ (TXB₂) in BALF, malondialdehyde (MDA) in the lungs, and activity of superoxide dismutase (SOD) in lung tissues were also determined.RESULTS:LPS induced acute lung injury, activated cPLA₂, and increased TXB₂ content in the BALF and MDA level in the lung tissue. The pretreatment with berberine significantly attenuated lung injury, lung edema and protein leakage induced by intraperitoneal injection of LPS. The expression of phospho-cPLA₂ in the lung tissues and TXB₂ content in the BALF in the berberine treatment group were lower than those in LPS group (P<0.05). In addition, the content of MDA in the lung tissue was lower in the berberine treatment group than LPS group (P<0.05), but there was no significant difference in activity of lung SOD between the berberine treatment and LPS group (P>0.05). CONCLUSION:Pretreatment with berberine remarkably reduces the LPS-induced lung injury, which is, at least in part, through inhibiting phosphorylation of cPLA₂ and decreasing lipid peroxidation. These findings provide a new strategy for the prevention and treatment of LPS-induced acute lung injury.