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右美托咪定对大鼠局灶性脑缺血再灌注时iNOS和COX-2表达的影响
张立功;赵津津;王公明;张孟元;王立俊
中华麻醉学杂志 2016年 36卷1期 页码:109-112页,共4页 影响因子:0.825
右美托咪啶;再灌注损伤;脑;一氧化氮合酶;环氧化酶-2
目的 评价右美托咪定对大鼠局灶性脑缺血再灌注时iNOS和环氧合酶-2(COX-2)表达的影响.方法 清洁级健康成年雄性SD大鼠30只,12~ 16月龄,体重300~ 360 g,采用随机数字表法分为3组(n=10):假手术组(Sham组)、局灶性脑缺血再灌注组(I/R组)和右美托咪定组(D组).采用右侧大脑中动脉闭塞法制备局灶性脑缺血再灌注损伤模型.D组于缺血1 h即刻经尾静脉注射右美托咪定1 μg/kg负荷剂量(注射时间10 min),然后以0.05 μg· kg-1·min-1的速率静脉输注至再灌注2h.于再灌注24 h时评价神经功能后处死大鼠取脑,测定脑梗死体积,计算脑梗死体积百分比,采用Western blot法检测海马iNOS和环氧合酶-2(COX-2)的表达.结果 与Sham组比较,I/R组和D组神经功能缺陷评分、左侧旋转次数百分比、脑梗死体积百分比及海马iNOS和COX-2表达水平升高(P<0.05);与I/R组比较,D组神经功能缺陷评分、左侧旋转次数百分比、脑梗死体积百分比及海马iNOS和COX-2表达水平降低(P<0.05).结论 右美托咪定减轻大鼠局灶性脑缺血再灌注损伤的机制可能与抑制iNOS和COX-2表达有关.
Subcellular localization of beta-arrestin1 and its prognostic value in lung adenocarcinoma
Li, XW;Che, KY;Wang, LG;Zhang, TH;Wang, GH;Pang, ZF;Shen, HC;Du, JJ
MEDICINE 2017年 96卷45期
NUCLEAR EXPORT SIGNAL; BETA-ARRESTINS; HIGH EXPRESSION; BREAST-CANCER; UNFAVORABLE PROGNOSIS; PROSTATE-CANCER; POOR-PROGNOSIS; P300; GROWTH; PROGRESSION
-Arrestins play important roles in cancer progression, and the subcellular localization of -arrestin1 has been receiving increasingly more attention. Intriguingly, several studies, including some of our previous work, showed that the effects of -arrestin1 on outcomes of cancer patients were controversial.Specimens were obtained from 133 patients with lung adenocarcinoma. Immunohistochemistry was used to detect the expression of -arrestin1 and p300 in the collected tissues. The Kaplan-Meier analysis and Cox proportional hazards regression were used to examine the relationship between -arrestin1 and patient survival.We found no significant association between -arrestin1 and clinicopathological variables. The Kaplan-Meier plot showed that patients with high expression of -arrestin1 (especially in the nucleus) had a poorer overall survival (OS) and shorter disease-free survival (DFS) (P=.026, P=.015). Additionally, high p300 expression also resulted in worse OS (P=.039). Following the univariate analysis, high expressions of nuclear -arrestin1 and p300 were classed as poor prognostic factors for both OS (P=.016) and DFS (P=.025).The expression of -arrestin1 in the nucleus is associated with increased malignant tendency of lung adenocarcinoma, and the predictive value of -arrestin1 may be optimized by combining information about the expression of p300 acetyltransferase.
Hollow double-layered polymer nanoparticles with S-nitrosothiols for tumor targeted therapy
Liu, TW;Hu, JJ;Ma, XY;Kong, B;Wang, JL;Zhang, ZD;Guo, DS;Yang, XL
JOURNAL OF MATERIALS CHEMISTRY B 2017年 5卷36期 页码:7519-7528
NITRIC-OXIDE RELEASE; DRUG-DELIVERY; PHENYLBORONIC ACID; ANTICANCER DRUG; CANCER-CELLS; STIMULI; GLUTATHIONE; DONOR; NO; NANOHYDROGELS
Tumor targeted hollow double-layered polymer nanoparticles (HDPNs) with S-nitrosothiols for nitric oxide (NO)-release as chemotherapy were described. Via a two-stage distillation precipitation co-polymerization, simple post-treatment and S-nitrosothiol modification, the S-nitroso HDPNs showed pH and glucose dual responsiveness. This would benefit accurate binding with the sialic acid over-expressed cancer cells, providing prerequisites for the disulfide polymer assisted cell uptake, intracellular GSH induced decomposition and rapid NO release. Confocal microscopy and cytotoxicity assay with normal versus tumor cells demonstrated in vitro recognition, intracellular delivery ability and tumor cell targeting cytotoxicity. Especially worth mentioning, the inevitable small amount of NO leakage in the transmission would take part in normal physiological activities and not cause serious side effects, providing a possible solution to avoid the intolerable side effects of traditional chemotherapy treatments for cancer.
Contribution of BDNF/TrkB signalling in the rACC to the development of pain-related aversion via activation of ERK in rats with spared nerve injury
Wang, X;Zhang, L;Zhan, YF;Li, DP;Zhang, YG;Wang, GM;Zhang, MY
BRAIN RESEARCH 2017年 1671卷 页码:111-120
ANTERIOR CINGULATE CORTEX; SPINAL DORSAL HORN; NEUROTROPHIC FACTOR; NEUROPATHIC PAIN; PROTEIN-KINASE; ANIMAL-MODEL; MAP KINASE; SYNAPTIC PLASTICITY; LIGATION MODEL; BACK-PAIN
The rostral anterior cingulate cortex (rACC) is a key structure in mediating the negative affective component of chronic pain. Brain-derived neurotrophic factor (BDNF) is known to play a critical role in activity dependent synaptic plasticity, learning and memory. It has been shown that BDNF signalling in the rACC might be involved in spontaneous pain-related aversion, but its underlying mechanism is still largely unknown. To address this question, we measured the mRNA and protein levels of BDNF in the rACC after nerve injury and found that BDNF expression was markedly higher in nerve-injured rats than in controls. Moreover, we found that conditioned place avoidance (CPA), a behavioural phenotype reflecting pain related aversion, was acquired in rats with partial sciatic nerve transection. However, a local injection of a BDNF-tropomyosin receptor kinase B (TrkB) antagonist into the rACC completely suppressed this process. Importantly, we found that administration of exogenous BDNF into the rACC of intact rats was sufficient to produce CPA, while selectively blocking phosphorylated extracellular signal regulated kinase (p-ERK) with a mitogen-activated protein kinase (MAPK) inhibitor U0126 completely abolished the acquisition of BDNF-induced CPA. In conclusion, we demonstrate, for the first time, that ERK is an important downstream effector of the BDNF/TrkB-mediated signalling pathway in the rACC that contributes to the development of neuropathic pain-related aversion. (C) 2017 Elsevier B.V. All rights reserved.
Morin Suppresses Astrocyte Activation and Regulates Cytokine Release in Bone Cancer Pain Rat Models
Jiang, W;Wang, Y;Sun, W;Zhang, MY
PHYTOTHERAPY RESEARCH 2017年 31卷9期 页码:1298-1304
SPINAL-CORD; NEUROPATHIC PAIN; CONSTRICTION INJURY; GLIAL ACTIVATION; OXIDATIVE STRESS; MECHANISMS; SENSITIZATION; HYPERALGESIA; INFLAMMATION; ALLODYNIA
As inflammatory and immune responses are involved in pathophysiology of debilitating neuropathic pain, reagents that can modulate these two responses may have therapeutic potential. Morin, derived from the moraceae family of plants, benefits inflammation-related diseases, but its antinociceptive effects on cancer pain remain elusive. In the present study, we investigated antinociceptive effects of morin on bone cancer pain using a rat model, where rats were subject to implantation of Walker 256 mammary gland carcinoma cells into the tibia. Morin (5-20mg/kg) dose-dependently attenuated behavioral hypersensitivities, including mechanical allodynia and free movement pain, which was accompanied by downregulation of astrocyte marker glial fibrillary acidic protein in the spinal cord in cancer-bearing rats. Treatment with morin also induced reduction of pro-inflammatory cytokines TNF-, IL-1, and IL-6 and upregulation of an antiinflammatory cytokine IL-10. Furthermore, intrathecal injection of AM630 (an antagonist of cannabinoid receptor 2, CB2), but not naloxone (an antagonist of opioid receptors), significantly blocked morin attenuation of behavioral hypersensitivities. Taken together, these results suggest that morin suppresses astrocyte activation and neuro-inflammation induced by bone cancer pain and its antinociceptive effects on bone cancer pain may be associated with activation of CB2 receptors in the spinal cord. Copyright (c) 2017 John Wiley & Sons, Ltd.
Paeoniflorin improves regional cerebral blood flow and suppresses inflammatory factors in the hippocampus of rats with vascular dementia
Zhang, LG;Wang, LJ;Shen, QQ;Wang, HF;Zhang, Y;Shi, CG;Zhang, SC;Zhang, MY
CHINESE JOURNAL OF INTEGRATIVE MEDICINE 2017年 23卷9期 页码:696-702
NF-KAPPA-B; IN-VIVO; IMPAIRMENT; ACTIVATION; MEMORY
To explore the delayed neuroprotection induced by paeoniflorin (PF), the principal component of Paeoniae radix prescribed in Chinese medicine, and its underlying mechanisms in rats subjected to vascular dementia (VD).;-;A rat model of VD was induced by bilateral common carotid arteries occlusion (BCCAO). Low-dose or high-dose PF (20 or 40 mg/kg once per day) was administrated for 28 days after VD. The behavioral analysis of rat was measured by water morris. Regional cerebral blood volume (rCBV), regional cerebral blood flflow (rCBF) and mean transit time (MTT) were measured in the bilateral hippocampus by perfusion-weighted imaging (PWI). The levels of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were measured by commercially available enzyme-linked immunosorbent assay kits. Protein levels were evaluated by western blot analysis. mRNA levels were evaluated by real time-polymerase chain reaction. Western blotting was used to estimate p65 translocation.;-;The behavioral analysis showed that PF could decrease the escape latency time (P < 0.05), and increase the residence time of the original platform quadrant and the across platform frequency in water maze in VD rats (P < 0.05). Likewise, PF remarkably promoted the rCBV (P < 0.05), rCBF and decreased per minute MTT (P < 0.05) in hippocampus of VD rats. Furthermore, PF decreased the release of IL-1 beta, IL-6 and TNF-alpha as well as inhibited the mRNA expression of IL-1 beta, IL-6 and TNF-alpha in the hippocampus of VD rats (P < 0.05 or P < 0.01). PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats (P < 0.05 or P < 0.01). In addition, PF signifificantly inhibited the nuclear factor kappa B (NF-kappa B) pathway in the hippocampus of VD rats.;-;PF signifificantly attenuates cognitive impairment, improves hippocampus perfusion and inhibits inflflammatory response in VD rats. In addition, the anti-inflflammatory effects of PF might be due to inhibiting the NF-kappa B pathway. PF may be a potential clinical application in improving VD.
Dexmedetomidine preconditioning plays a neuroprotective role and suppresses TLR4/NF-kappa B pathways model of cerebral ischemia reperfusion
Wang, SL;Duan, L;Xia, B;Liua, ZF;Wang, Y;Wang, GM
BIOMEDICINE & PHARMACOTHERAPY 2017年 93卷 页码:1337-1342
MOUSE MODEL; OXIDATIVE STRESS; INJURY; RATS; INFLAMMATION; PROTECTION; ACTIVATION; EXPRESSION
Background: Dexmedetomidine has been reported to play an efficient role on multi-organ protection. Our study aims to investigate the neuroprotective of dexmedetomidine preconditioning on cerebral ischemic reperfusion (I/R) injury and investigate the underlining signaling mechanisms.;-;Methods: Cerebral I/R models were established with SD rats through middle cerebral artery occlusion (MCAO). After 2 h of ischemia followed by 7 days of reperfusion, the degree of cerebral tissue injury was detected by HE, Nissl and TUNEL staining. Glial fibrillary acidic protein (GFAP) positive and TNF-alpha positive cells were stained by immunohistochemistry and counted under microscope. TLR4, NF-kappa B and TIR-domain containing adapter-inducing interferon-beta (TRIF) expression were detected by real time PCR and western blot.;-;Results: Dexmedetomidine preconditioning markedly prevented the ischemia-induced cellular damage observed from HE and Nissl staining in hippocampus and cortex. Dexmedetomidine observably decreased the number of apoptotic cells in TUNEL staining. Besides, yohimbine could specifically suppress the protective effect of dexmedetomidine. GFAP expression was distinctly inhibited by dexmedetomidine preconditioning (10 mu g/kg, 20 mu g/kg) in cerebral ischemia area. Dexmedetomidine preconditioning inhibited the expression of TLR4 and NF-kappa B and increased that of TRIF.;-;Conclusion: The results of this study suggest that dexmedetomidine preconditioning plays a neuroprotective role against I/R injury. Dexmedetomidine might suppress TLR4/NF-??B pathway and drive TLR4/TRIF signaling pathway to reduce the inflammatory injury. (C) 2017 Elsevier Masson SAS. All rights reserved.
Pancreaticoduodenectomy for duodenal papilla carcinoma: A single-centre 9-year retrospective study of 112 patients with long-term follow-up
Lian, PL;Chang, Y;Xu, XC;Zhao, Z;Wang, XQ;Xu, KS
WORLD JOURNAL OF GASTROENTEROLOGY 2017年 23卷30期 页码:5579-5588
PYLORUS-PRESERVING PANCREATICODUODENECTOMY; PERIAMPULLARY CANCER; VATER; AMPULLA; TUMORS; METAANALYSIS; RESECTION; PANCREAS; SURGERY; REGION
AIM;-;To retrospectively evaluate the factors that influence long-term outcomes of duodenal papilla carcinoma (DPC) after standard pancreaticoduodenectomy (SPD).;-;METHODS;-;This is a single-centre, retrospective study including 112 DPC patients who had a SPD between 2006 and 2015. Associations between serum levels of CA19-9 and CEA and various clinical characteristics of 112 patients with DPC were evaluated by the. 2 test and Fisher's exact test. The patients were followed-up every 3 mo in the first two years and at least every 6 mo afterwards, with a median follow-up of 60 mo (ranging from 4 mo to 168 mo). Survival analysis was conducted using the Kaplan-Meier survival and Cox proportional hazards model analysis. The difference in survival curves was evaluated with a log-rank test.;-;RESULTS;-;In 112 patients undergoing SPD, serum levels of CA19-9 was associated with serum levels of CEA and drainage mode (the P values were 0.000 and 0.033, respectively); While serum levels of CEA was associated with serum levels of CA19-9 and differentiation of the tumour (the P values were 0.000 and 0.033, respectively). The serum levels of CA19-9 and CEA were closely correlated (chi(2) = 13.277, r = 0.344, P = 0.000). The overall 5-year survival was 50.00% for 112 patients undergoing SPD. The Kaplan-Meier survival analysis showed that increased serum levels of CA19-9, CEA, and total bilirubin were correlated with a poor prognosis, as well as a senior grade of infiltration depth, lymph node metastases, and TNM stage(the P values were 0.033, 0.018, 0.015, 0.000, 0.000 and 0.000, respectively). Only the senior grade of infiltration depth and TNM stage retained their significance when adjustments were made for other known prognostic factors in Cox multivariate analysis (RR = 2.211, P = 0.022 and RR = 2.109, P = 0.047).;-;CONCLUSION;-;For patients with DPC, the serum levels of CA19-9 and CEA were closely correlated, and play an important role in poor survival. Increased serum levels of total bilirubin and lymph node metastases were also correlated with a poor prognosis. The senior grade of infiltration depth and TNM stage can serve as independent prognosis indexes in the evaluation of patients with DPC after SPD.
Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-kappa B and Inflammation Response
Wang, LJ;Liu, HY;Zhang, LG;Wang, GM;Zhang, MY;Yu, YH
BIOMOLECULES & THERAPEUTICS 2017年 25卷4期 页码:383-389
GLOBAL-ISCHEMIA; BRAIN-INJURY; SIGNALING PATHWAY; OXIDATIVE STRESS; ARTERY OCCLUSION; NEONATAL-RATS; EXPRESSION; TRANSIENT; ACTIVATION; NEURODEGENERATION
Dexmedetomidine is an alpha 2-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induded cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of 1 mu g/kg load dose, followed by 0.05 mu g/kg/min infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-1 beta, interleukin-6 and tumor nevrosis factor-alpha as well as the protein expression of inducible nitric Oxide synthase, cyclooxygenase-2, nuclear factor-kappa Bp65, inhibitor of kappa B alpha and phosphorylated of kappa B alpha in hippocampus were asessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-kappa B pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.
Protective effect of propofol preconditioning on ischemia-reperfusion injury in human hepatocyte
Zhang, YZ;Chen, ZZ;Feng, NH;Tang, JX;Zhao, XB;Liu, CX;Xu, HY;Zhang, MY
JOURNAL OF THORACIC DISEASE 2017年 9卷3期 页码:702-710
OXIDATIVE STRESS; CELL-DEATH; PARTIAL-HEPATECTOMY; CEREBRAL-ISCHEMIA; HEPATIC-INJURY; LIVER-INJURY; RAT MODEL; IN-VIVO; APOPTOSIS; DISEASE
Background: Blood reperfusion after ischemia is the main measure to restore cell function. This study was aimed to explore the effect of propofol on rat and cell models of liver ischemia-reperfusion (I/R) injury, and to investigate its possible mechanism.;-;Methods: Wistar rats were divided into four groups: control group, sham group, I/R group, and propofol group. Human hepatocyte HL7702 was divided into six groups: control group, I/R group and propofol (5, 10, 20 and 40 mu mol/L) groups. After the animal and cell models were established, the alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA) and adenosine triphosphate (ATP) levels in liver tissues and hepatocytes were measured. Cell viability and apoptosis of hepatocytes were respectively determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Furthermore, the expressions of apoptosis-related proteins in hepatocytes were determined by Western blot analysis.;-;Results: ALT, AST and MDA levels were all decreased significantly, and the ATP level was increased significantly in propofol group compared with that in I/R group in both liver tissues and hepatocytes. Additionally, cell viability of hepatocytes in propofol group was higher than that in I/R group, while the percentage of apoptotic cells in propofol group was less than that in I/ R group. Moreover, the expression of caspase-3 decreased and the expression of Bcl-2 increased significantly after propofol preconditioning.;-;Conclusions: Our findings suggested that propofol preconditioning might be an effective strategy for protecting the liver from I/ R injury, which might provide a scientific basis for clinical application.
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