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1.
比较了芪蓝抗毒饮三种剂量和中剂量三种给药次数对雏鸡实验性传染性法氏囊病的疗效。结果表明,中剂量和发病后该剂量每天给药1次、连续4天的疗效最好。  相似文献   
2.
实验性脾虚证大白鼠酶组织化学研究   总被引:1,自引:0,他引:1  
将45只大白鼠随机分成3组,即实验组、治疗组及对照组,每组15只。以利血平致大白鼠脾虚证模型,分阶段捕杀动物,取肝脏、胃、十二指肠,用酶组织化学方法测定酸性磷酸酶(ACP)、碱性磷酸酶(ALP)、葡萄糖-6-磷酸酶(G-6-Pase)活性的变化。结果表明:实验组、治疗组、正常对照组各酶活性均发生了变化,在第7天、第14天时组内各酶存在着动态学上的变化。治疗组各酶活性接近正常对照组,说明四君子汤具明显的治疗作用。  相似文献   
3.
AIM:To observe the effects of Sini decoction on atherosclerosis(AS) and ceramide content of aorta in rabbits. METHODS:28 rabbits were randomly divided into three groups. Control group was fed with a normal diet; High cholesterol group was fed 1% cholesterol and 5% fat diet; Sini decotion+ high cholesterol group was fed 1% cholesterol and 5% fat diet plus Sini decotion (4.2 g·kg-1·d-1). At the end of study, the plaque area were measured, the atorta ceramide and cell apoptosis were also detected. RESULTS:Sini decotion diminished lipid plaque area on the aortic endothelium, reduced the levels of aorta ceramide and the apoptosis index. CONCLUSION:Sini decoction has an inhibitory effect on AS, the mechanism may be that Sini decotion reduces concentration of ceramide in aorta.  相似文献   
4.
AIM: To investigate the influence of Sini decoction (SND) on the proliferation and apoptosis of rabbit abdominal aorta smooth muscle cells after ballon injury and discuss the effect of vascular smooth muscle cell's (VSMCs) proliferation and apoptosis in post-percutaneous coronary intervention (PCI) restenosis (RS) and the feasibility of SND preventing post-PCI RS. METHODS: The animal model of rabbit abdominal aorta ballon injury was set up and the therapertic group was treated with SND. The shape of proliferative and apoptotic cell were investigated by electron microscope. Immunohistochemistry staining was performed using α-actin,PCNA and Cyclin E monoclonal antibodies. In situ Cell Death Detection Kit was used to identify apoptotic cells. Abdomial aorta angiography was operated in the 84th day subgroup and the stenosis degree was evalued by quantitative angiographic analysis. RESULTS: As compared with the control group, the therapeutic group displayed a lower proliferative percentage and a higher apoptosic percentage (P<0.05). Moreover, the apoptosic peek time was on the 14th day after operation,which was longer than the control group. CONCLUSION: SND effectly inhibited the proliferation of VSMCs and iuduced apoptosis in VSMCs.  相似文献   
5.
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.  相似文献   
6.
15头健康仔猪,分3组,每组5头:即健康组、脾虚组和四君子汤反证组。按20mg/kg的剂量内服进行左旋氧氟沙星的辨证药动学研究。高效液相色谱法测定血浆中药物浓度,3p97药代动力学程序处理药时数据。健康组和脾虚组药动学数据符合一级吸收一室模型,四君子汤反证组药动学数据符合一级吸收二室模型。试验结果表明:仔猪脾虚状态下明显影响左旋氧氟沙星内服给药的药动学特征(PK);四君子汤可使脾虚仔猪异常的左旋氧氟沙星的药动学特征得到恢复,为验证“辨证药动学”假说和完善中西兽医结合提供了进一步的科学依据。  相似文献   
7.
MA Wei  YANG Jia-yao  AN Liu  ZOU Qi  ZHANG Xiao  LIU Nian 《园艺学报》2021,36(12):2258-2263
AIM To observe the effect of Fuzilizhong decoction on the inflammatory damage of non-alcoholic fatty liver disease (NAFLD) rats and to explore its mechanism. METHODS SPF male SD rats were randomly divided into 6 groups: control group, model group, high dose (20 mg·kg-1·d-1), middle dose (10 mg·kg-1·d-1), low dose (5 mg·kg-1·d-1) Fuzilizhong decoction group and Yishanfu (30 mg·kg-1·d-1)group, 8 rats in each group. A NAFLD rat modelwas established by intragastric administration of fat emulsion for 4 weeks. Then the drug was given for 4 weeks in each treatment group. HE staining was performed to observe the histopathological changes of the rat liver.The serum levels of interleukin-2(IL-2), IL-6 and tumor necrosis factor-α(TNF-α) were measured by ELISA. The expression of toll like receptor 4(TLR4) and NF-κB p65 in liver tissues at mRNA and protein levels was determined by RT-qPCR and Western bolt,respectively. RESULTS Compared with control group, the inflammatory damage of liver tissue was more serious, the serum levels of IL-2, IL-6 and TNF-α, the mRNA expression TLR4 and NF-κB p65 in liver tissues were significantly increased in model group(P<0.05). However, compared with model group, the liver pathological changes in each treatment group were significantly relieved, the serum levels of IL-2, IL-6 and TNF-α, the mRNA expression of TLR4 and NF-κB p65 in liver tissues were significantly reduced(P<0.05).In addition, the changes of TLR4 and p-NF-κB p65 protein levels in liver tissue were consistent with the changes of TLR4 and NF-κB p65 mRNA. CONCLUSION Fuzilizhong decoction attenuates the inflammatory damages of NAFLD in rats by inhibiting TLR4/NF-κB p65 signaling pathway.  相似文献   
8.
目的:考察菊楂决明饮中山楂、决明子(炒决明子)、菊花配伍单煎液与共煎液的化学成分及抗氧化活性差异。方法:采用紫外分光光度法测定总黄酮、总蒽醌的含量;采用酸碱滴定法测定总酸的含量;采用HPLC法测定山楂酸、大黄酚、橙黄决明素、绿原酸、木犀草苷、3,5-O-双咖啡酰基奎宁酸的含量。结果:山楂单煎液的总黄酮含量为 {1.63% }、总酸含量为5.44%、山楂酸含量为2.37%、对DPPH自由基的清除率为46.49%;决明子单煎液的总黄酮含量为0.54%、总蒽醌含量为0.27%、大黄酚含量为0.14%、橙黄决明素含量为 {0.52% }、对DPPH自由基的清除率为3.53%;炒决明子单煎液的总黄酮含量为0.52%、总蒽醌含量为0.29%、大黄酚含量为0.22%、橙黄决明素含量为0.56%、对DPPH自由基的清除率为25.07%;菊花单煎液的总黄酮含量为1.65%、绿原酸含量为 {0.99% }、木犀草苷含量为 {0.30% }、3,5-O-双咖啡酰基奎宁酸含量为2.65%、对DPPH自由基的清除率为45.89%;山楂、决明子、菊花共煎液总黄酮含量为2.62%、总酸含量为 {4.12% }、总蒽醌含量为0.25%、山楂酸含量为1.25%、大黄酚含量为0.16%、橙黄决明素含量为0.56%、绿原酸含量为 {3.01% }、木犀草苷含量为0.48%、3,5-O-双咖啡酰基奎宁酸含量为3.97%、对DPPH自由基的清除率为25.92%;山楂、炒决明子、菊花共煎液总黄酮含量为2.56%、总酸含量为 {3.94% }、总蒽醌含量为0.24%、山楂酸含量为0.43%、大黄酚含量为0.33%、橙黄决明素含量为1.00%、绿原酸含量为4.12%、木犀草苷含量为 {0.60% }、3,5-O-双咖啡酰基奎宁酸含量为4.74%、对DPPH自由基的清除率为44.51%。结论:山楂、决明子、菊花共煎后,与单煎液相比,总黄酮、大黄酚、橙黄决明素、绿原酸、木犀草苷、3,5-O-双咖啡酰基奎宁酸含量均升高;总酸、总蒽醌、山楂酸含量都有不同程度降低,对DPPH自由基清除率与单煎液相当。  相似文献   
9.
目的 探讨在高糖作用下,体外培养的小鼠足细胞凋亡及bax、bcl-2表达水平的变化,及左归降糖益肾方含药血浆的调控作用。方法 将体外培养的小鼠足细胞随机分为空白组(A组,25 mmoL/L葡萄糖,10%空白血浆)、高糖组(B组,200 mmoL/L葡萄糖,10%空白血浆)、左归降糖益肾方含药血浆组(C组,200 mmoL/L葡萄糖,10%含药血浆),4-苯基丁酸(4-PBA)含药血浆组(D组,200 mmoL/L葡萄糖,10%含药血浆)。采用间接免疫荧光细胞化学法检测足细胞凋亡情况;MTT自动比色法检测足细胞活力,蛋白质印迹法和逆转录-聚合酶链反应法分别检测bax及bcl-2蛋白或mRNA表达水平的变化。结果 与A组相比,B组足细胞活力降低,bax及 bcl-2蛋白或mRNA的表达水平均升高(P<0.01);与B组相比,C组、D组足细胞活力升高,bax蛋白或mRNA的表达水平均降低(P<0.05或P<0.01),bcl-2蛋白或mRNA的表达水平均升高(P<0.01);与C组比,D组足细胞活力升高(P<0.05),但bax及bcl-2蛋白或mRNA的表达水平,差异均无统计学意义(P>0.05)。结论 bax及bcl-2蛋白或mRNA表达水平的升高,是足细胞损伤的分子机制之一;左归降糖益肾方含药血浆可以通过影响bax及bcl-2蛋白或mRNA的表达水平,从而抑制足细胞凋亡。  相似文献   
10.
目的 探讨加味丹参饮(JDSH)预处理对大鼠心肌缺血再灌注损伤(IRI)的保护作用及机制。方法 采用结扎大鼠冠状动脉左前降支30 min后再灌注30/60 min模型,将56只SD雄性大鼠随机分为7组:假手术组、缺血/再灌注(I/R)30 min组、I/R 60 min组、p38MAPK阻断剂SB203580+I/R 30 min组、SB203580+I/R 60 min组、JDSH+I/R 30 min组、JDSH+I/R60 min组。各组干预2 d后,HE染色心肌组织标本,全自动生化分析仪测定血清CK、LDH,免疫组化法检测p38MAPK、COX-2和ICAM-1蛋白的表达。结果 经JDSH预处理或p38MAPK阻断剂SB203580处理后心肌细胞形态结构保持更好。与假手术组比较,I/R30 min组和I/R 60min组大鼠血清中的CK、LDH明显升高(P<0.01);与I/R 30/60 min比较,SB203580+I/R 30/60 min组和JDSH+I/R 30/60 min组均明显降低(P<0.01)。与假手术组比较,I/R使大鼠心肌组织的p38MAPK、COX-2、ICAM-1蛋白表达增加(P<0.01),且随再灌注时间的延长而增加;与I/R 30/60 min组比较,SB203580和JDSH均能减少其蛋白表达(P<0.01)。结论 大鼠心肌IRI时,激活了p38MAPK信号通路,且与再灌注时间(30~60 min)呈正相关。JDSH通过抑制p38MAPK信号通路,降低其下游基因COX-2和ICAM-1的表达,降低CK、LDH,减轻心肌损伤,起到保护心肌作用。  相似文献   
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