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1. Reduced Nicotinamide Adenine Dinucleotide Phosphate Inhibits Platelet Function | |||
Gu Yi,Qin Zhenghong | |||
Basic Medicine 07 March 2018 | |||
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Abstract:Background-In previous studies, the protection of reduced nicotinamide adenine dinucleotide phosphate (NADPH) on neurons against ischemia/reperfusion-induced injury was determined and its inhibition on platelet aggregation was found by accident. Here, the function of NADPH on platelet is explored deeply. Methods and Results-In vitro studies, the effects of different concentrations of NADPH on platelet aggregation induced by ADP (10 μM), thrombin (0.05 U/mL) or AA (0.5 mM) were determined and we found that NADPH could concentration-dependently inhibit platelet aggregation induced by ADP or thrombin. When the inhibitory effects of NAD+, NADH, NADP+ and NADPH on platelet aggregation were compared, NADPH showed the best effect. In vivo studies, the effects between NADPH and aspirin on tail bleeding time, clotting time and ferric chloride-induced thrombosis model were compared in mice or rats. NADPH could prolong the tail bleeding times in mice, especially at 30 min after the injection of NADPH (7.5 mg/kg), while bleeding times in mice given aspirin (15 mg/kg) were significantly longer at any time point in 6 h. As we detected the influence of NADPH or aspirin on clotting times in rats, we found that both of them had no effect. Using a FeCl3-induced abdominal aorta injury thrombosis model, we found that the injection of NADPH provoked a significant time delay of vessel occlusion, while aspirin almost completely prevented the vessel occlusion. After we observed the injured vessel sections under the microscope, we discovered that the thrombi in injured vessel sections of rats injected NADPH were much looser than rats injected normal saline and the thrombi in injured vessel sections of rats given aspirin were fewest. Conclusions-The current results suggest that NADPH can inhibit platelet aggregation and prevent hemostasis and thrombosis. To our knowledge, this is the first study on the effect of NADPH on platelet function. | |||
TO cite this article:Gu Yi,Qin Zhenghong. Reduced Nicotinamide Adenine Dinucleotide Phosphate Inhibits Platelet Function[OL].[ 7 March 2018] http://en.paper.edu.cn/en_releasepaper/content/4743750 |
2. Nuclear translocation of DJ-1 protects the adult neuronal stem cells in MPTP-induced mouse Parkinson's disease model | |||
SUN Yi,WANG Yupeng,LIN Yuanbin,ZHAO Xin,PU Xiaoping | |||
Basic Medicine 21 April 2017 | |||
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Abstract:The DJ-1 gene, originally identified as an oncogene, is a causative gene for a familial form of Parkinson's disease (PD), PARK7. DJ-1 protein was found to play multiple roles in various physiological and pathological processes including cellular transformation, regulating oxidative stress and transcription, as well as cell growth and death. We found previously that DJ-1 was closely associated with the proliferation and differentiation of cultured neuronal stem cells. In this study, we further investigated other functions of DJ-1, in an attempt to determine how adult neurogenesis was affected in the subgranular zones (SGZ), the subventricular zone (SVZ) and olfactory bulb (OB), the brain areas closely related to early non-motor symptoms of PD, using an MPTP-induced mouse PD model. The results demonstrated that the number of BrdU+ cells in SGZ for both MPTP-treated and saline control groups were not significantly different. However, increased migration of BrdU+ cells into the olfactory glomerulus layer of OB was observed 14 days after MPTP injection, suggesting a compensatory mechanism might exist to restore neuronal loss. Specifically, we found that DJ-1 was translocated into the nuclei of the BrdU+ cells in SGZ and SVZ, but not in OB. A plausible explanation is that the nuclear translocation of DJ-1 mainly occurs in the early stages of adult NSCs proliferation in vivo. However, within the BrdU- cells in the olfactory glomerulus layer of OB, DJ-1 was concentrated into nuclei. These results indicated that the nuclear translocation of DJ-1 might be involved in maintaining the olfactory function of mature olfactory neurons. The research presented here thus provided evidence on using DJ-1 as a tool and biomarker for PD early diagnosis, stratification and possibly therapeutic treatments. | |||
TO cite this article:SUN Yi,WANG Yupeng,LIN Yuanbin, et al. Nuclear translocation of DJ-1 protects the adult neuronal stem cells in MPTP-induced mouse Parkinson's disease model[OL].[21 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4725748 |
3. NMDA receptor blockade suppresses pentylenetetrazole-induced acute seizure and kindling | |||
Yong Qianye,Li Shujun,Wang Huize,Kong Lingwen,Li Siqi,Zhu Xinjian | |||
Basic Medicine 11 October 2016 | |||
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Abstract:N-methyl-D-aspartate (NMDA) receptor plays an important role in the pathophysiology of several neurological diseases, including epilepsy. The present study, therefore, using the non-competitive NMDA receptor antagonist, MK-801 to investigate the role of NMDA receptor in pentylenetetrazole (PTZ)-induced kindling and the possible cellular and molecular mechanisms involved. Our results showed that acute seizure was induced in male C57BL/6 mice with a single dose of PTZ (60mg/kg), while kindling was induced with a subconvulsive dose of PTZ (35mg/kg) for at least 9 injections. Blocking NMDA receptor by non-competitive antagonist MK-801, however, significantly suppressed PTZ-induced acute seizure and the development of kindling. These results indicate that PTZ-induced acute seizure and kindling are dependent on NMDA receptor activation. | |||
TO cite this article:Yong Qianye,Li Shujun,Wang Huize, et al. NMDA receptor blockade suppresses pentylenetetrazole-induced acute seizure and kindling[OL].[11 October 2016] http://en.paper.edu.cn/en_releasepaper/content/4705952 |
4. Chinese Herbal Medicine and Alzheimer Disease | |||
TAN Yan,LI Jiao,LIANG Mi,HUA Qian | |||
Basic Medicine 24 May 2016 | |||
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Abstract:Chinese herbal medicine (CHM) has a long history in oriental countries. Its characteristics refer to four properties, five flavors, and meridian tropisms. The medical practice of CHM is based on the principles of traditional Chinese medicine (TCM), such as holism, yin-yang theory, Zang-fu system and the five elements, so called Zheng in total. For its therapeutic benefits with relation to brain diseases, such as stroke, Alzheimer's disease (AD), CHM can be dated from 2,500 years ago. In addition, under the guidance of Zheng, there are two mainly causes leading to the on-set of Alzheimer disease (AD) - the deficiency of kidney qi and phlegm-dampness blocking cystitis. Therefore, driven by Zheng, we list two typical Chinese herbal formulae in the treatment of AD, and its mechanisms. | |||
TO cite this article:TAN Yan,LI Jiao,LIANG Mi, et al. Chinese Herbal Medicine and Alzheimer Disease[OL].[24 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4691222 |
5. Discussion on the Calculation of Absolute Bioavailability | |||
Jiang Wei,Yang Juan-juan,Cao Lei,Shi Xiao-lian,Cao Yong-xiao* | |||
Basic Medicine 18 April 2015 | |||
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Abstract:The absolute bioavailability (F) is defined as the ratio of drug amounts between being absorbed and the total amount of drug being administrated one after extravascular administration. It is calculated as the ratio of area under plasma drug concentration-time curve (AUC) between the extravascular administration and the intravenous injection. However, the distribution of a drug after intravenous administration does not reach balance in the body when the plasma drug concentration declines sharp at the distribution phase. Therefore, at this phase plasma drug concentration can't reflect the total drug amount in body. The goal of the present investigation was to analyze its insufficient and give a modification. The literatures about absolute bioavailability were searched by the keyword "absolute bioavailability" in "Pubmed" from 1983 to 2014. The data on plasma drug concentration were obtained from literatures directly or recovered from the concentration-time curve by Microsoft Paint. The plasma drug concentrations were calculated at each time point at the distribution phase according to the plasma drug concentration-time relationship at elimination phase, which represent the drug amount in body. The AUC basing on the drug concentrations in distribution balance after intravenous injection was 75%±11% of the one basing on actual measured drug concentrations in literatures. The absolute bioavailability from the literatures was 76%±12% of the actual one basing on the AUC from distribution balanced drug concentrations. Therefore, the present method underestimating absolute bioavailability should be corrected. | |||
TO cite this article:Jiang Wei,Yang Juan-juan,Cao Lei, et al. Discussion on the Calculation of Absolute Bioavailability[OL].[18 April 2015] http://en.paper.edu.cn/en_releasepaper/content/4638715 |
6. Evaluation of Scutellaria barbata D.Don ethanol extract and its components on antitumor effects of low dose 5-fluorouracil against hepatocellular carcinoma cells | |||
XU Huanli,DU Guanhua | |||
Basic Medicine 30 December 2014 | |||
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Abstract:Background: Some compounds derived from Chinese medicine have demonstrated prospective roles in sensitization to chemotherapy. Aim: This study aimed to investigate Scutellaria barbata D.Don ethanol extract (SBEE) and its components on antitumor effects of low dose 5-fluorouracil against hepatocellular carcinoma cells. Methods: The antitumor effects of SBEE and its components, and their combinations with 5-FU were detected by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium/phenazine methosulfate assay, and the effects of drug combinations were evaluated using Jin's formula. Results:SBEE and luteolin could inhibit tumor growth in time and dose dependent manners. Drug combination study showed that SBEE and luteolin could synergize the antitumor effects of 5-fluorouracil at different dose ratios against HepG2 and Bel-7402 cells.Conclusion: SBEE and luteolin showed synergistic antitumor effects when combined with low dose 5-FU, and the mechanism of the synergistic effect remains to be to be studied. | |||
TO cite this article:XU Huanli,DU Guanhua. Evaluation of Scutellaria barbata D.Don ethanol extract and its components on antitumor effects of low dose 5-fluorouracil against hepatocellular carcinoma cells[OL].[30 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4625638 |
7. Decreased carboxylesterases expression and hydrolytic activity in type 2 diabetic mice through Akt/mTOR/HIF-1α/ Stra13 pathway | |||
Chen Ruini,Wang Yuwen,Ning Rui,Liu Wei,Xiong Jing,Yang Jian | |||
Basic Medicine 05 December 2014 | |||
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Abstract:Carboxylesterases constitute a class of enzymes that hydrolyze drugs containing such functional groups as esters, amides, thioesters and carbamates. Ljver has abundant carboxylesterases expression, however, the alteration of carboxylesterases in type 2 diabetes remains to be elucidated. In this study, type 2 diabetic (T2D) mice were prepared by combination of high-fat diet and streptozocin (STZ) injection. We found that the carboxylesterase 1d (Ces1d, CES1) and carboxylesterase 1e (Ces1e, CES2) expression and the capacity of hydrolytic activity of liver and intestine decreased, whereas the Akt/mTOR/HIF-1α/ Stra13 (DEC1) signaling was activated in T2D mice. Consistently, high insulin could come out the same results in high glucose DMEM condition, which mimicked T2D, in primary mouse hepatocytes. Perifosine or rapamycin almost abolished the decreases of Ces1d and Ces1e expression and hydrolytic activity induced by insulin in the primary mouse hepatocytes. Moreover, the responsiveness of human hepatoma (HepG2) cells to high insulin in high glucose condition was similar to the primary mouse hepatocytes in terms of altered expression of carboxylesterases. Knockdown of HIF-1α or DEC1 with shRNA construct abrogated the decreases of CES1 and CES2 expression induced by insulin. The data suggest that the decreased carboxylesterases expression and hydrolytic activity in T2D mice are through Akt/mTOR/HIF-1α/Stra13 (DEC1) pathway. The findings will contribute to guide rational use of drugs in type 2 diabetic patients. | |||
TO cite this article:Chen Ruini,Wang Yuwen,Ning Rui, et al. Decreased carboxylesterases expression and hydrolytic activity in type 2 diabetic mice through Akt/mTOR/HIF-1α/ Stra13 pathway[OL].[ 5 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4620177 |
8. Xylocarpin H, a component of Xylocarpus granatum, produces antidepressant-like activities in mice | |||
YIN Xi,LI Xin,HAO Yaoguang,ZHAO Yiwen,ZHOU Jinghong,SHI Haishui | |||
Basic Medicine 26 November 2014 | |||
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Abstract:Major depression is a common psychiatric disorder worldwide that imposes a substantial health burden on society. Currently available antidepressants do not meet the clinical needs. Here, we report that Xylocarpin H, an active component of Xylocarpus granatum, has antidepressant-like effects in mouse models of depression. In mouse forced swimming- and tail suspension tests, two validated models of depression, oral administration of Xylocarpin H resulted in a dose-dependent decreased immobility duration within the dose range of 15-50 mg/kg. In addition, Xylocarpin H dose-dependently increased the time in the central zone at doses of 5-50 mg/kg in the locomotion activity test. The antidepressant-like activities of Xylocarpin H were associated with its inhibitory effects on hypothalamic-pituitary-adrenal (HPA) axis' hyperactivity in response to acute stress. Interestingly, these effective doses of Xylocarpin H did not affect locomotor- and HPA axis activities in the absence of stress. In summary, the present study, for the first time, demonstrated that Xylocarpin H exerts antidepressant-like effects in mouse behavioral models of depression, likely by inhibiting HPA axis systems. These data provide a strong basis for developing Xylocarpin H as a novel antidepressant agent for the treatment of major depression disorders. | |||
TO cite this article:YIN Xi,LI Xin,HAO Yaoguang, et al. Xylocarpin H, a component of Xylocarpus granatum, produces antidepressant-like activities in mice[OL].[26 November 2014] http://en.paper.edu.cn/en_releasepaper/content/4620567 |
9. Cardiac-specific BMP4 transgenic mice does not develop a pathological heart hypertrophy phenotype because of immaturity of the overexpressed BMP4 | |||
Yonghui Zhang,Ning Ma,Shan-Liang Li,Rong Huo,Bo Sun,Yue Sheng,Feng Cheng,Xue-Ting Du,De-Li Dong | |||
Basic Medicine 08 November 2014 | |||
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Abstract: Background/Aims: Our previous work showed that bone morphogenetic protein 4 (BMP-4) induced cardiomyocyte hypertrophy. In the present work, we established the transgenic mice (TG) with cardiac-specific overexpression of BMP4 and investigated whether these transgenic mice could develop a pathological heart hypertrophy phenotype or show exacerbated pathological heart hypertrophy under pressure-overload stimulus. Methods: Transgenic mice with cardiac-specific overexpression of BMP4 were identified by PCR and western blot analysis. The pressure-overload heart hypertrophy was induced by transverse aortic constriction (TAC) operation. Cardiac function was assessed by echocardiography using a Visual- Sonics Vevo 2100 Imaging System. Results: TG mice expressed significantly higher protein level of BMP4 precursor form but not the mature form. TG mice did not develop a pathological heart hypertrophy phenotype at 16 weeks after birth. Pressure-overload for 4 weeks induced significant heart hypertrophy in both TG and wild type (WT) mice, but there was no difference in the hypertrophic parameters between TG and WT mice treated with pressure-overload. Pressure-overload induced significant increase of BMP4 expression in protein level in both TG and WT mice, but no difference of BMP4 mature form was observed between TG and WT mice treated with pressure-overload. Conclusion: The increased precursor form in cardiac BMP4 TG mice did not become matured even under the pressure-overload stimulus, so these transgenic mice could not develop a pathological heart hypertrophy phenotype or show exacerbated pathological heart hypertrophy under pathological stimuli. | |||
TO cite this article:Yonghui Zhang,Ning Ma,Shan-Liang Li, et al. Cardiac-specific BMP4 transgenic mice does not develop a pathological heart hypertrophy phenotype because of immaturity of the overexpressed BMP4[OL].[ 8 November 2014] http://en.paper.edu.cn/en_releasepaper/content/4614634 |
10. Glaucocalyxin A induces apoptosis in human squamous cell carcinoma KB cellsthrough lysosomal-mitochondrial death pathway | |||
Sun Lingmei,Liao Kai | |||
Basic Medicine 09 January 2014 | |||
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Abstract:Glaucocalyxin A (GLA) is a biologically active ent-kauranoid diterpenoid isolated from Rabdosia japonicavar glaucocalyx, a traditional Chinese medicinal herb, which has been shown to inhibit tumor cell proliferation. Our results showed that GLA is a powerful growth inhibitor of K562, PC3, MCF-7 and KB cancer cells, IC50 ranged from 3~8.4 μM. Cell flow cytometry of GLA-treated KB cells showed a marked accumulation of cells in the S-phase and G2-phase fraction in a dose-dependent manner. In addition, staining for annexin V/PI, changes in nuclear morphology, and activation of caspase-9 and -3 support a role for apoptosis. Further investigation with squamous cell carcinoma KB cells found that GLA could induce an early lysosomal rupture within 6h as assessed by acridine-orange uptake. Additional experiments revealed that GLA could induce a dose-dependent accumulation of reactive oxygen species (ROS), trigger mitochondrial membrane permeabilization, release cytochrome c, and then down-regulate Bcl-2, up-regulate Bax. These results revealed that the cytoxicity of GLA was involved in a lysosomal-mitochondrial death pathwan | |||
TO cite this article:Sun Lingmei,Liao Kai. Glaucocalyxin A induces apoptosis in human squamous cell carcinoma KB cellsthrough lysosomal-mitochondrial death pathway[OL].[ 9 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4581415 |
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