17 results on '"Cao, Jiang"'
Search Results
2. Development and validation of a nomogram to predict postoperative delirium in older patients after major abdominal surgery: a retrospective case-control study
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Luo, Yun-Gen, Wu, Xiao-Dong, Song, Yu-Xiang, Wang, Xiao-Lin, Liu, Kai, Shi, Chun-Ting, Wang, Zi-Lin, Ma, Yu-Long, Li, Hao, Liu, Yan-Hong, Mi, Wei-Dong, Lou, Jing-Sheng, and Cao, Jiang-Bei
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- 2024
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3. Analysis of endophytic bacterial diversity in seeds of different genotypes of cotton and the suppression of Verticillium wilt pathogen infection by a synthetic microbial community
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Wu, Chong-Die, Fan, Yong-Bin, Chen, Xue, Cao, Jiang-Wei, Ye, Jing-Yi, Feng, Meng-Lei, Liu, Xing-Xing, Sun, Wen-Jing, Liu, Rui-Na, and Wang, Ai-Ying
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- 2024
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4. Radiosynthesis of a novel antisense imaging probe targeting LncRNA HOTAIR in malignant glioma
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Ren, Jiongyu, Zhang, Xiyuan, Cao, Jiang, Tian, Jiali, Luo, Jin, Yu, Yaping, Wang, Fengkui, and Zhao, Qian
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- 2022
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5. Effectiveness of Tirobot-assisted vertebroplasty in treating thoracolumbar osteoporotic compression fracture
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Wang, Boyao, Cao, Jiang, Chang, Jie, Yin, Guoyong, Cai, Weihua, Li, Qingqing, Huang, Zhenfei, Yu, Lipeng, and Cao, Xiaojian
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- 2021
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6. High expression of miR-25 predicts favorable chemotherapy outcome in patients with acute myeloid leukemia
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Niu, Mingshan, Feng, Yuan, Zhang, Ninghan, Shao, Tingting, Zhang, Huihui, Wang, Rong, Yao, Yao, Yao, Ruosi, Wu, Qingyun, Cao, Jiang, Liu, Xuejiao, Liu, Yubo, and Xu, Kailin
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- 2019
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7. High expression of miR-363 predicts poor prognosis and guides treatment selection in acute myeloid leukemia
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Zhang, Huihui, Zhang, Ninghan, Wang, Rong, Shao, Tingting, Feng, Yuan, Yao, Yao, Wu, Qingyun, Zhu, Shengyun, Cao, Jiang, Zhang, Huanxin, Li, Zhenyu, Liu, Xuejiao, Niu, Mingshan, and Xu, Kailin
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- 2019
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8. MiR-425 expression profiling in acute myeloid leukemia might guide the treatment choice between allogeneic transplantation and chemotherapy
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Yang, Chen, Shao, Tingting, Zhang, Huihui, Zhang, Ninghan, Shi, Xiaoying, Liu, Xuejiao, Yao, Yao, Xu, Linyan, Zhu, Shengyun, Cao, Jiang, Cheng, Hai, Yan, Zhiling, Li, Zhenyu, Niu, Mingshan, and Xu, Kailin
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- 2018
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9. BMCMDA: a novel model for predicting human microbe-disease associations via binary matrix completion
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Shi, Jian-Yu, Huang, Hua, Zhang, Yan-Ning, Cao, Jiang-Bo, and Yiu, Siu-Ming
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- 2018
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10. Effectiveness of Tirobot-assisted vertebroplasty in treating thoracolumbar osteoporotic compression fracture
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Qingqing Li, Zhenfei Huang, Cao Jiang, Guoyong Yin, Weihua Cai, Wang Boyao, Xiaojian Cao, Lipeng Yu, and Chang Jie
- Subjects
musculoskeletal diseases ,Male ,medicine.medical_specialty ,lcsh:Diseases of the musculoskeletal system ,Percutaneous ,Robot ,Thoracic Vertebrae ,03 medical and health sciences ,0302 clinical medicine ,Postoperative Complications ,lcsh:Orthopedic surgery ,Robotic Surgical Procedures ,Fractures, Compression ,medicine ,Humans ,Orthopedics and Sports Medicine ,Clinical efficacy ,Compression fracture ,Vas score ,Aged ,Retrospective Studies ,Aged, 80 and over ,030222 orthopedics ,Vertebroplasty ,Lumbar Vertebrae ,business.industry ,Retrospective cohort study ,Middle Aged ,Radiation Exposure ,Compression (physics) ,medicine.disease ,Thrombosis ,Surgery ,lcsh:RD701-811 ,Treatment Outcome ,Fluoroscopy ,Orthopedic surgery ,Female ,lcsh:RC925-935 ,business ,030217 neurology & neurosurgery ,Osteoporotic Fractures ,Cement leakage ,Research Article - Abstract
BackgroundPercutaneous kyphoplasty is the main method in the treatment of thoracolumbar osteoporotic compression fractures. However, much radiation exposure during the operation harms the health of surgeons and patients. In addition, the accuracy of this surgery still needs to be improved. This study aimed to assess the radiation exposure and clinical efficacy of Tirobot-assisted vertebroplasty in treating thoracolumbar osteoporotic compression fracture.MethodsIncluded in this retrospective cohort study were 60 patients (60–90 years) who had undergone unilateral vertebroplasty for thoracolumbar osteoporotic compression fracture at our hospital between June 2019 and June 2020. All showed no systemic diseases and were assigned to Tirobot group (treated with Tirobot-assisted approach) and control group (treated with traditional approach). Fluoroscopic frequency, operative duration, length of stay (LOS), post-operative complications (cement leakage, infection, and thrombosis), and pre-operative and pre-discharge indexes (VAS score, JOA score, and Cobb’s angle) were compared.ResultsThe fluoroscopic frequency (P< 0.001) and post-operative complications (P= 0.035) in Tirobot group were significantly lower than those in control group. The operative duration and LOS in the Tirobot group were shorter than those in the control group, but the differences were not statistically significant (P= 0.183). Pre-discharge VAS score and Cobb’s angle decreased, and JOA increased after surgeries in both groups. These three indexes showed a significant difference after surgery in each group (P< 0.001), but not between groups (PVAS= 0.175,PCobb’s= 0.585,PJOA= 0.448).ConclusionThe Tirobot-assisted vertebroplasty can reduce surgery-related trauma, post-operative complications, and patients’ and operators’ exposure to radiation. As a safe and effective strategy, this surgery can realize the quick recovery from thoracolumbar osteoporotic compression fracture.
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- 2021
11. Acetaminophen attenuates lipopolysaccharide-induced cognitive impairment through antioxidant activity.
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Wei-Xing Zhao, Jun-Han Zhang, Cao Jiang-Bei, Wei Wang, Dong-Xin Wang, Xiao-Ying Zhang, Jun Yu, Yong-Yi Zhang, You-Zhi Zhang, Wei-Dong Mi, Zhao, Wei-Xing, Zhang, Jun-Han, Cao, Jiang-Bei, Wang, Wei, Wang, Dong-Xin, Zhang, Xiao-Ying, Yu, Jun, Zhang, Yong-Yi, Zhang, You-Zhi, and Mi, Wei-Dong
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ACETAMINOPHEN ,LIPOPOLYSACCHARIDES ,MILD cognitive impairment ,MICROINJECTIONS ,NEUROPROTECTIVE agents ,ANIMAL experimentation ,ANIMALS ,ANTIOXIDANTS ,HIPPOCAMPUS (Brain) ,LEARNING ,MICE ,MOTOR ability ,PHARMACODYNAMICS - Abstract
Background: Considerable evidence has shown that neuroinflammation and oxidative stress play an important role in the pathophysiology of postoperative cognitive dysfunction (POCD) and other progressive neurodegenerative disorders. Increasing evidence suggests that acetaminophen (APAP) has unappreciated antioxidant and anti-inflammatory properties. However, the impact of APAP on the cognitive sequelae of inflammatory and oxidative stress is unknown. The objective of this study is to explore whether APAP could have neuroprotective effects on lipopolysaccharide (LPS)-induced cognitive impairment in mice.Methods: A mouse model of LPS-induced cognitive impairment was established to evaluate the neuroprotective effects of APAP against LPS-induced cognitive impairment. Adult C57BL/6 mice were treated with APAP half an hour prior to intracerebroventricular microinjection of LPS and every day thereafter, until the end of the study period. The Morris water maze was used to assess cognitive function from postinjection days 1 to 3. Animal behavioural tests as well as pathological and biochemical assays were performed to evaluate LPS-induced hippocampal damage and the neuroprotective effect of APAP.Results: Mice treated with LPS exhibited impaired performance in the Morris water maze without changing spontaneous locomotor activity, which was ameliorated by treatment with APAP. APAP suppressed the accumulation of pro-inflammatory cytokines and microglial activation induced by LPS in the hippocampus. In addition, APAP increased SOD activity, reduced MDA levels, modulated glycogen synthase kinase 3β (GSK3β) activity and elevated brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Moreover, APAP significantly decreased the Bax/Bcl-2 ratio and neuron apoptosis in the hippocampus of LPS-treated mice.Conclusions: Our results suggest that APAP may possess a neuroprotective effect against LPS-induced cognitive impairment and inflammatory and oxidative stress via mechanisms involving its antioxidant and anti-inflammatory properties, as well as its ability to inhibit the mitochondrial permeability transition (MPT) pore and the subsequent apoptotic pathway. [ABSTRACT FROM AUTHOR]- Published
- 2017
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- View/download PDF
12. Single nucleotide polymorphisms in apoptosis pathway are associated with response to imatinib therapy in chronic myeloid leukemia.
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Qiaoli Zheng, Jiang Cao, Hamad, Nada, Hyeoung-Joon Kim, Joon Ho Moon, Sang Kyun Sohn, Chul Won Jung, Lipton, Jeffrey H., Dong Hwan Kim, Dennis, Zheng, Qiaoli, Cao, Jiang, Kim, Hyeoung-Joon, Moon, Joon Ho, Sohn, Sang Kyun, Jung, Chul Won, and Kim, Dennis Dong Hwan
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SINGLE nucleotide polymorphisms ,APOPTOSIS ,DRUG therapy ,IMATINIB ,TREATMENT of chronic myeloid leukemia ,ANTINEOPLASTIC agents ,CELLULAR signal transduction ,DEMOGRAPHY ,FUNCTIONAL assessment ,GENETIC polymorphisms ,MULTIVARIATE analysis ,PROGNOSIS ,RESEARCH evaluation ,CHRONIC myeloid leukemia ,TREATMENT effectiveness ,GENOTYPES - Abstract
Background: The mechanism of action of imatinib is known to involve the Fas-mediated apoptosis pathway. Consequently inter-individual variations in this apoptosis pathway might be associated with imatinib response or resistance.Methods: This study attempted to focus on eight genotypes in the apoptosis pathway including FAS (rs1800682, rs2229521, rs2234767 and rs2234978), FASLG (rs763110), CASP10 (rs13006529), and APAF1 (rs1439123, rs2288713) and analyzed their association with treatment outcomes including molecular response with 4.5 log reduction (MR4.5), following imatinib therapy in 187 Korean CML patients.Results: The GG/GA genotype in FAS (rs2234767) showed a higher rate of MR4.5 than the AA genotype (at 5 years 59.7 vs 37.4 %, p = 0.013). Using a bootstrap procedure for internal validation we confirmed that FAS (rs2234767) correlates with MR4.5 (p = 0.050). Multivariate analysis confirmed that the FAS genotype (rs2234767) is an independent surrogate for MR4.5 (p = 0.019, HR 0.43, 95 % CI [0.22-0.87]).Conclusions: The Fas/FasL signaling pathway may represent the major pathway that mediates apoptosis in CML treated with imatinib. SNP markers in the apoptosis pathway including FAS genotype (rs2234767) can be potential surrogates for predicting deeper molecular response after imatinib therapy. [ABSTRACT FROM AUTHOR]- Published
- 2016
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- View/download PDF
13. The therapeutic target of estrogen receptor-alpha36 in estrogen-dependent tumors.
- Author
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Gu, Yu, Chen, Tianxiang, López, Elena, Wu, Weizhu, Wang, Xiangdong, Cao, Jiang, and Teng, Lisong
- Abstract
Estrogen receptor-alpha36 (ER-α36) is a new isoform of estrogen receptors without transcriptional activation domains of the classical ER-α(ER - α66). ER-α36 is mainly located in cytoplasm and plasma membrane. ER-α36 mediates non-genomic signaling and is involved in genomic signaling of other ERs. Recently ER-α36 is found to play a critical role in the development of estrogen-dependent cancers and endocrine resistance of breast cancer. The present article overviews and updates the biological nature and function of ER-α36, potential interaction of ER-α36 with other estrogen receptors and growth factor receptors, intracellular signaling pathways, potential mechanism by which ER-α36 may play an important role in the development of tumor resistance to endocrine therapies. [ABSTRACT FROM AUTHOR]
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- 2014
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14. Acetaminophen attenuates lipopolysaccharide-induced cognitive impairment through antioxidant activity.
- Author
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Zhao WX, Zhang JH, Cao JB, Wang W, Wang DX, Zhang XY, Yu J, Zhang YY, Zhang YZ, and Mi WD
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- Animals, Lipopolysaccharides toxicity, Male, Maze Learning drug effects, Mice, Mice, Inbred C57BL, Motor Activity drug effects, Neuroprotective Agents pharmacology, Acetaminophen pharmacology, Antioxidants pharmacology, Cognitive Dysfunction chemically induced, Hippocampus drug effects
- Abstract
Background: Considerable evidence has shown that neuroinflammation and oxidative stress play an important role in the pathophysiology of postoperative cognitive dysfunction (POCD) and other progressive neurodegenerative disorders. Increasing evidence suggests that acetaminophen (APAP) has unappreciated antioxidant and anti-inflammatory properties. However, the impact of APAP on the cognitive sequelae of inflammatory and oxidative stress is unknown. The objective of this study is to explore whether APAP could have neuroprotective effects on lipopolysaccharide (LPS)-induced cognitive impairment in mice., Methods: A mouse model of LPS-induced cognitive impairment was established to evaluate the neuroprotective effects of APAP against LPS-induced cognitive impairment. Adult C57BL/6 mice were treated with APAP half an hour prior to intracerebroventricular microinjection of LPS and every day thereafter, until the end of the study period. The Morris water maze was used to assess cognitive function from postinjection days 1 to 3. Animal behavioural tests as well as pathological and biochemical assays were performed to evaluate LPS-induced hippocampal damage and the neuroprotective effect of APAP., Results: Mice treated with LPS exhibited impaired performance in the Morris water maze without changing spontaneous locomotor activity, which was ameliorated by treatment with APAP. APAP suppressed the accumulation of pro-inflammatory cytokines and microglial activation induced by LPS in the hippocampus. In addition, APAP increased SOD activity, reduced MDA levels, modulated glycogen synthase kinase 3β (GSK3β) activity and elevated brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Moreover, APAP significantly decreased the Bax/Bcl-2 ratio and neuron apoptosis in the hippocampus of LPS-treated mice., Conclusions: Our results suggest that APAP may possess a neuroprotective effect against LPS-induced cognitive impairment and inflammatory and oxidative stress via mechanisms involving its antioxidant and anti-inflammatory properties, as well as its ability to inhibit the mitochondrial permeability transition (MPT) pore and the subsequent apoptotic pathway.
- Published
- 2017
- Full Text
- View/download PDF
15. Single nucleotide polymorphisms in apoptosis pathway are associated with response to imatinib therapy in chronic myeloid leukemia.
- Author
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Zheng Q, Cao J, Hamad N, Kim HJ, Moon JH, Sohn SK, Jung CW, Lipton JH, and Kim DD
- Subjects
- Adolescent, Adult, Aged, Aged, 80 and over, Child, Demography, Female, Genotype, Humans, Imatinib Mesylate pharmacology, Male, Middle Aged, Multivariate Analysis, Prognosis, Reproducibility of Results, Treatment Outcome, Young Adult, Apoptosis genetics, Imatinib Mesylate therapeutic use, Leukemia, Myelogenous, Chronic, BCR-ABL Positive drug therapy, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, Polymorphism, Single Nucleotide genetics, Signal Transduction genetics
- Abstract
Background: The mechanism of action of imatinib is known to involve the Fas-mediated apoptosis pathway. Consequently inter-individual variations in this apoptosis pathway might be associated with imatinib response or resistance., Methods: This study attempted to focus on eight genotypes in the apoptosis pathway including FAS (rs1800682, rs2229521, rs2234767 and rs2234978), FASLG (rs763110), CASP10 (rs13006529), and APAF1 (rs1439123, rs2288713) and analyzed their association with treatment outcomes including molecular response with 4.5 log reduction (MR4.5), following imatinib therapy in 187 Korean CML patients., Results: The GG/GA genotype in FAS (rs2234767) showed a higher rate of MR4.5 than the AA genotype (at 5 years 59.7 vs 37.4 %, p = 0.013). Using a bootstrap procedure for internal validation we confirmed that FAS (rs2234767) correlates with MR4.5 (p = 0.050). Multivariate analysis confirmed that the FAS genotype (rs2234767) is an independent surrogate for MR4.5 (p = 0.019, HR 0.43, 95 % CI [0.22-0.87])., Conclusions: The Fas/FasL signaling pathway may represent the major pathway that mediates apoptosis in CML treated with imatinib. SNP markers in the apoptosis pathway including FAS genotype (rs2234767) can be potential surrogates for predicting deeper molecular response after imatinib therapy.
- Published
- 2016
- Full Text
- View/download PDF
16. DNA Polymerases as targets for gene therapy of hepatocellular carcinoma.
- Author
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Liu H, Wei Q, Wang J, Huang X, Li C, Zheng Q, Cao J, and Jia Z
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- Adenoviridae genetics, Animals, Apoptosis genetics, Carcinoma, Hepatocellular pathology, Carcinoma, Hepatocellular therapy, Cell Line, Tumor, DNA Polymerase I antagonists & inhibitors, DNA Polymerase II antagonists & inhibitors, DNA Polymerase III antagonists & inhibitors, Genetic Therapy, Humans, Liver Neoplasms pathology, Liver Neoplasms therapy, Mice, MicroRNAs genetics, Molecular Targeted Therapy, Promoter Regions, Genetic, Xenograft Model Antitumor Assays, Carcinoma, Hepatocellular genetics, DNA Polymerase I genetics, DNA Polymerase II genetics, DNA Polymerase III genetics, Liver Neoplasms genetics
- Abstract
Background: Hepatocyte carcinoma (HCC) is one of the most common malignancies worldwide. Despite many achievements in diagnosis and treatment, HCC mortality remains high due to the malignant nature of the disease. Novel approaches, especially for targeted therapy, are being extensively explored. Gene therapy is ideal for such purpose for its specific expression of exogenous genes in HCC cells driven by tissue-specific promoter. However strategies based on correction of mutations or altered expressions of genes responsible for the development/progression of HCC have limitations because these aberrant molecules are not presented in all cancerous cells. In the current work, we adopted a novel strategy by targeting the DNA replication step which is essential for proliferation of every cancer cell., Methods: A recombinant adenovirus with alpha fetoprotein (AFP) promoter-controlled expressions of artificial microRNAs targeting DNA polymerases α, δ, ε and recombinant active Caspase 3, namely Ad/AFP-Casp-AFP-amiR, was constructed., Results: The artificial microRNAs could efficiently inhibit the expression of the target polymerases in AFP-positive HCC cells at both RNA and protein levels, and HCC cells treated with the recombinant virus Ad/AFP-Casp-AFP-amiR exhibited significant G0/1 phase arrest. The proliferation of HCC cells were significantly inhibited by Ad/AFP-Casp-AFP-amiR with increased apoptosis. On the contrary, the recombinant adenovirus Ad/AFP-Casp-AFP-amiR did not inhibit the expression of DNA polymerases α, δ or ε in AFP-negative human normal liver cell HL7702, and showed no effect on the cell cycle progression, proliferation or apoptosis., Conclusions: Inhibition of DNA polymerases α, δ and ε by AFP promoter-driven artificial microRNAs may lead to effective growth arrest of AFP-positive HCC cells, which may represent a novel strategy for gene therapy by targeting the genes that are essential for the growth/proliferation of cancer cells, avoiding the limitations set by any of the individually altered gene.
- Published
- 2015
- Full Text
- View/download PDF
17. Deferoxamine attenuates lipopolysaccharide-induced neuroinflammation and memory impairment in mice.
- Author
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Zhang XY, Cao JB, Zhang LM, Li YF, and Mi WD
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- Animals, Caspase 3 metabolism, Disease Models, Animal, Dose-Response Relationship, Drug, Encephalitis chemically induced, Encephalitis complications, Exploratory Behavior drug effects, Glycogen Synthase Kinase 3 metabolism, Glycogen Synthase Kinase 3 beta, Interleukin-1beta metabolism, Iron metabolism, Lipopolysaccharides toxicity, Male, Malondialdehyde metabolism, Maze Learning drug effects, Memory Disorders chemically induced, Memory Disorders etiology, Mice, Mice, Inbred C57BL, Reaction Time drug effects, Superoxide Dismutase metabolism, Tumor Necrosis Factor-alpha metabolism, Deferoxamine therapeutic use, Encephalitis drug therapy, Memory Disorders prevention & control, Siderophores therapeutic use
- Abstract
Background: Neuroinflammation often results in enduring cognitive impairment and is a risk factor for postoperative cognitive dysfunction. There are currently no effective treatments for infection-induced cognitive impairment. Previous studies have shown that the iron chelator deferoxamine (DFO) can increase the resistance of neurons to injury and disease by stimulating adaptive cellular stress responses. However, the impact of DFO on the cognitive sequelae of neuroinflammation is unknown., Methods: A mouse model of lipopolysaccharide (LPS)-induced cognitive impairment was established to evaluate the neuroprotective effects of DFO against LPS-induced memory deficits and neuroinflammation. Adult C57BL/6 mice were treated with 0.5 μg of DFO 3 days prior to intracerebroventricular microinjection of 2 μg of LPS. Cognitive function was assessed using a Morris water maze from post-injection days 1 to 3. Animal behavioral tests, as well as pathological and biochemical assays were performed to evaluate the LPS-induced hippocampal damage and the neuroprotective effect of DFO., Results: Treatment of mice with LPS resulted in deficits in cognitive performance in the Morris water maze without changing locomotor activity, which were ameliorated by pretreatment with DFO. DFO prevented LPS-induced microglial activation and elevations of IL-1β and TNF-α levels in the hippocampus. Moreover, DFO attenuated elevated expression of caspase-3, modulated GSK3β activity, and prevented LPS-induced increases of MDA and SOD levels in the hippocampus. DFO also significantly blocked LPS-induced iron accumulation and altered expression of proteins related to iron metabolism in the hippocampus., Conclusions: Our results suggest that DFO may possess a neuroprotective effect against LPS-induced neuroinflammation and cognitive deficits via mechanisms involving maintenance of less brain iron, prevention of neuroinflammation, and alleviation of oxidative stress and apoptosis.
- Published
- 2015
- Full Text
- View/download PDF
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