全文获取类型
收费全文 | 668篇 |
免费 | 35篇 |
国内免费 | 71篇 |
专业分类
林业 | 1篇 |
农学 | 18篇 |
20篇 | |
综合类 | 138篇 |
农作物 | 44篇 |
水产渔业 | 13篇 |
畜牧兽医 | 167篇 |
园艺 | 341篇 |
植物保护 | 32篇 |
出版年
2024年 | 5篇 |
2023年 | 18篇 |
2022年 | 48篇 |
2021年 | 64篇 |
2020年 | 76篇 |
2019年 | 128篇 |
2018年 | 103篇 |
2017年 | 33篇 |
2016年 | 51篇 |
2015年 | 44篇 |
2014年 | 32篇 |
2013年 | 46篇 |
2012年 | 25篇 |
2011年 | 16篇 |
2010年 | 16篇 |
2009年 | 7篇 |
2008年 | 11篇 |
2007年 | 4篇 |
2006年 | 5篇 |
2005年 | 6篇 |
2004年 | 3篇 |
2003年 | 4篇 |
2002年 | 2篇 |
2000年 | 20篇 |
1997年 | 1篇 |
1962年 | 1篇 |
1956年 | 4篇 |
1955年 | 1篇 |
排序方式: 共有774条查询结果,搜索用时 31 毫秒
21.
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. 相似文献
22.
23.
为探讨山羊MC1R基因c.676A>G突变与山羊皮肤色素沉积的关系,及其对黑色素合成和cAMP信号通路下游色素相关基因表达的影响:一方面采用直接测序法检测酉州乌羊及其杂交后代群体(120个个体)MC1R基因c.676A>G的突变情况,用色差仪测量不同基因型个体的腹部皮肤色度值,分析c.676A>G突变与皮肤色素沉积的关系;另一方面,构建野生型(MC1R c.676A)和突变型(MC1R c.676G)真核表达载体,采用脂质体介导法转染到小鼠皮肤黑色素瘤细胞(B16-F10)中进行过表达,利用酶标仪检测各组细胞黑色素含量的差异,并通过实时荧光定量PCR方法检测各组细胞中cAMP信号通路下游色素相关基因(MITF、TYR、TYRP1、DCT)的表达差异性。结果显示:酉州乌羊及其杂交后代群体中,c.676A>G位点均以GG基因型占优势,不同基因型群体的皮肤色度值差异不显著(P>0.05)。MC1R突变组(MC1R c.676G)细胞中的黑色素含量极显著(P<0.05)高于MC1R野生组(MC1R c.676A)。MITF、TYRP1和DCT基因在MC1R突... 相似文献
24.
AIM To study the effect of dihydroartemisinin (DHA) on the radiotherapy efficiency in hepatocellular carcinoma H22 cell tumor-bearing mice and the role of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in this process. METHODS A model of H22 cell tumor-bearing mice was established. The mice was divided into model group, single radiotherapy group, 5-fluorouracil (5-FU) group, and low-, medium- and high-dose DHA groups. The body weight and tumor volume in each group were measured every other day. At the end of administration, blood was collected from the tail of the mice and the animals were killed by neck removal immediately. The synergistic effect of DHA on radiotherapy was determined, and tumor growth inhibitory rate was calculated. The degree of lymphocyte transformation and natural killer (NK) cell activity were measured by MTT, the serum levels of interleukin-2 (IL-2) and IL-4 were measured by ELISA, and the protein levels of PI3K, AKT and p-AKT were determined by Western blot. RESULTS The H22 cell tumor-bearing mouse model was successfully constructed. Compared with model group, the TGT3 (tumor growth time to reach 3 times of volume) of single radiotherapy group was remarkably increased (P <0.05), while tumor weight, lymphocyte transformation degree, NK cell activity, IL-2 and IL-4 levels, PI3K protein level and AKT phosphorylation level were remarkably decreased (P <0.05). Compared with single radiotherapy group, TGT3, EF (enhancement factor), tumor inhibitory rate, lymphocyte transformation degree, NK cell activity, IL-2 level and IL-4 level were increased with the increase in DHA dose (P <0.05), and the PI3K protein level and AKT phosphorylation level were decreased (P <0.05). CONCLUSION DHA may enhance the immunity of tumor-bearing mice by inhibiting the activity of PI3K/AKT signaling pathway, thereby enhancing the efficacy of radiotherapy. 相似文献
25.
AIM: To investigate the regulatory effect of JAK2-STAT3 signaling pathway on the neuroprotection of ischemic postconditioning (IPoC) in tree shrews, and to explore the mechanisms of cerebral injury deterioration after inhibiting the JAK2-STAT3 pathway. METHODS: The model of thrombotic cerebral ischemia was induced by photochemical reaction in tree shrews and the IPoC was established at 4 h after ischemia followed by clipping ipsilateral common carotid artery on the ischemia side for 5 min (3 times). After IPoC and intracerebroventricular injection of AG490 (JAK2 inhibitor), the changes of cerebral infarction area were detected by TTC staining, and the histological and ultrastructural changes of cortical neurons were observed under light and electron microscopes, respectively. The protein levels of t-STAT3 and p-STAT3 in the cortical tissue were determined by Western blot. RESULTS: The neuronal pycnosis, mitochondrial swelling and vanish of the mitochondrial cristae were found in cortical cortex, and the infarction area was (24.78±3.30)% at 24 h after cerebral ischemia. Meanwhile, the phosphorylation level of STAT3 protein in the cortical tissue was significantly increased (P<0.01). The cortical neuronal damage and mitochondrial swelling were decreased after IPoC, the area of cerebral infarction was significantly reduced to (17.67±1.83)% (P<0.01), and the phosphorylation level of STAT3 protein was further increased (P<0.01). However, the neuronal damage was aggravated, the infarction area was expanded to (23.85±2.77)%(P<0.05) after treatment with AG490, and the phosphorylation level of STAT3 protein was also significantly reduced (P<0.05). CONCLUSION: IPoC may reduce cerebral injury by regulating the phosphorylation of STAT3 protein, and inhibition of JAK2-STAT3 signaling pathway may counteract the cerebral protective effect of IPoC and aggravate brain injury. 相似文献
26.
JIAO Peng HUANG Zhen-zhou ZHANG Xiao-jing LONG Yan-jun LI Zhao-jun WANG Feng-ze 《园艺学报》2019,35(2):260-266
AIM:To investigate the effect of CUDC-907, a dual histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K) inhibitor, on the DNA damage, cell cycle distribution and autophagy in human glioma U251 cells. METHODS:U251 cells were treated with CUDC-907 of different concentrations, and the cell viability was detected by MTT assay. The quantitative γ-H2AX foci were determined by laser scanning confocal microscopy. The cell cycle distribution of U251 cells was examined by flow cytometry. The protein expression was determined by Western blot analysis. RESULTS:CUDC-907 inhibited the cell viability and the phosphorylation of Akt and p70 ribosomal protein S6 kinase (p70s6K) in the U251 cells (P<0.05). In CUDC-907-treated cells, the number of γ-H2AX foci and protein expression of γ-H2AX were increased significantly (P<0.05). CUDC-907 also induced cell arrest in the G2/M phase by up-regulating the expression of p21, and inhibiting the protein level of cyclin B1 and the phosphorylation of cell division cycle protein 2 (Cdc2). In addition, CUDC-907 triggered cell autophagy, and inhibition of autophagy increased CUDC-907-induced DNA damage of U251 cells. CONCLUSION:CUDC-907 significantly inhibits PI3K/Akt signaling pathway, induces DNA damage and arrests cell cycle in G2/M phase. Blockage of autophagy promotes CUDC-907-induced DNA damage of U251 cells. 相似文献
27.
AIM: To study the effect of fibroblast growth factor receptor 1 (FGFR1) expression knock-down on the viability, apoptosis, invasion and migration of infantile hemangioma endothelial cells (HemECs). METHODS: FGFR1 was down-regulated by FGFR1 small interfering RNA (si-FGFR1) transfection. The viability of the cells was measured by CCK-8 assay. The apoptotic rate was analyzed by flow cytometry and the invasion and migration abilities were determined by Transwell assay. The protein levels of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), and phosphorylated AKT (p-AKT) were examined by Western blot. RESULTS: Transfection of si-FGFR1 into HemECs had significant effects on inhibiting cell viability (P<0.05), promoting apoptosis (P<0.05), and decreasing cell invasion and migration abilities (P<0.05). The results of Western blot showed that knockdown of FGFR1 gene expression in the cells reduced the protein levels of PI3K and p-AKT (P<0.05), and had no significant effect on AKT protein level. CONCLUSION: Knock-down of FGFR1 expression changes the biological characteristics of endothelial cells in infantile hemangiomas by regulating PI3K/AKT signaling pathway. 相似文献
28.
CHEN Meng-yue CHEN Wei-dong LIU Yi-min XIANG Si-cheng YIN Hui-ling ZHANG Zhi-feng 《园艺学报》2019,35(1):106-111
AIM: To explore the effect of shikonin on rat primary cortical neurons in oxygen-glucose deprivation (OGD)-induced injury model.METHODS: The neurons were pretreated with shikonin at different concentrations (0.02, 0.2, 2 and 20 μmol/L) followed by treatment with OGD. Lactate dehydrogenase (LDH) release assay and fluorescein diacetate/propidium iodide (FDA/PI) double staining were used to detect neuronal viability and apoptosis, and then the optimal concentration of shikonin was determined. LY294002 (PI3K/Akt signaling pathway inhibitor, 1 μmol/L) was added before the addition of shikonin, and the protein level of p-Akt (Ser473) in the neurons was determined by Wes-tern blot. LDH release assay and FDA/PI double staining were also used to detect neuronal viability and apoptosis.RESULTS: A certain concentration (0.2~20 μmol/L) of shikonin increased the viability of impaired neurons (P<0.05) and the protein level of p-Akt (Ser473) in the neurons (P<0.05). The effect of shikonin on neuronal p-Akt (Ser473) levels and the cell death were blocked by LY294002 (P<0.05).CONCLUSION: A certain concentration of shikonin reduces OGD-induced apoptosis of rat primary cortical neurons by activating PI3K/Akt signaling pathway. 相似文献
29.
AIM: To explore the effect of tanshinone ⅡA on human osteosarcoma HOS cells and the underlying mechanism.METHODS: The cell viability and the appropriate dose of tanshinone ⅡA were determined by CCK-8 assay. Colony formation assay and Transwell assay were used to investigate the proliferation and migration abilities of the HOS cells treated with tanshinone ⅡA. The apoptosis of the HOS cells was monitored by Hoechst 33258 staining, transmission electron microscopy and flow cytometry. The protein levels of apoptosis-related molecules and JNK signaling-associated proteins were determined by Western blot. Meanwhile, a JNK inhibitor was added for confirming the relationship between the pathway and apoptosis mentioned above.RESULTS: Tanshinone ⅡA inhibited both HOS cell proliferation and migration in a dose-and time-dependent manner. Exposure of the HOS cells to tanshinone ⅡA resulted in the activation of apoptosis. Tanshinone ⅡA treatment increased the protein levels of cleaved caspase-3, Bax and JNK signaling-associated proteins, and decreased the protein level of Bcl-2, which were reversed by JNK inhibitor SP600125. Moreover, the result of CCK-8 assay revealed that tanshinone ⅡA-induced cell death was alleviated by JNK inhibitor.CONCLUSION: Tanshinone ⅡA induces cell growth inhibition and the activation of apoptosis via JNK signaling pathway in human osteosarcoma HOS cells. 相似文献
30.
LI Ming-hang TIAN Xiao-cui AN Rui-di ZHANG Qian YANG Mei XIANG Fei WANG Yu-chun XU Lu DONG Zhi 《园艺学报》2019,35(1):112-118
AIM: To investigate the effect of all-trans retinoic acid (ATRA) on blood-brain barrier after cerebral ischemia-reperfusion (CIR) injury in rats and its possible role mechanism.METHODS: Male SD rats were randomly divided into sham group, model (CIR) group and CIR+ATRA (10, 30 and 90 mg/kg) groups. The rat model of CIR injury was established by MCAO thread occlusion method. After ischemia for 1.5 h and reperfusion for 24 h, the neurological functional behavioral score, cerebral infarction volume, brain water content and Evans blue content were determined. The activity of matrix metalloprotein-9 (MMP-9) was measured by gelatin zymography. The protein levels of claudin-5, occludin, ZO-1, JNK, p-JNK, P38, p-P38 and MMP-9 in the brain tissues were determined by Western blot.RESULTS: Compared with CIR model group, ATRA at 30 mg/kg significantly improved neurological function, and decreased cerebral infarction volume, brain water content, Evans blue content and the degradation of tight junction proteins in ischemic area (P<0.01). The activity and protein expression of MMP-9 in ischemic brain tissue were decreased (P<0.01). The phosphorylation of JNK and P38 was inhibited and the protein levels of p-JNK and p-P38 were decreased (P<0.01).CONCLUSION: ATRA reduces the damage of brain tissue and the destruction of blood-brain barrier induced by CIR in rats. The protective effect may be related to inhibiting the activation of JNK/P38 MAPK signaling pathway and MMP-9. 相似文献