7 results on '"Zhang, Mingkun"'
Search Results
2. Metabolite differences between glutamate carboxypeptidase II gene knockout mice and their wild-type littermates after traumatic brain injury: a 7-tesla 1H-MRS study
- Author
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Wu, Wenbo, Xu, Siyi, Wang, Jialin, Zhang, Kuiming, Zhang, Mingkun, Cao, Yang, Ren, Hongqing, Zheng, Deyou, and Zhong, Chunlong
- Published
- 2018
- Full Text
- View/download PDF
3. Astaxanthin protects astrocytes against trauma-induced apoptosis through inhibition of NKCC1 expression via the NF-κB signaling pathway.
- Author
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Mingkun Zhang, Zhenwen Cui, Hua Cui, Yong Wang, Chunlong Zhong, Zhang, Mingkun, Cui, Zhenwen, Cui, Hua, Wang, Yong, and Zhong, Chunlong
- Subjects
ASTAXANTHIN ,CAROTENOIDS ,ASTROCYTES ,APOPTOSIS prevention ,TUMOR necrosis factors ,PHYSIOLOGY ,ANIMALS ,APOPTOSIS ,CELL culture ,CELLS ,CELLULAR signal transduction ,MICE ,XANTHOPHYLLS ,DNA-binding proteins ,NEUROPROTECTIVE agents ,ION transport (Biology) ,PHARMACODYNAMICS - Abstract
Background: Astaxanthin (ATX) is a carotenoid pigment with pleiotropic pharmacological properties that is seen as a possible drug for treating cerebral ischemic injury and subarachnoid hemorrhage. Na+-K+-2Cl- co-transporter-1 (NKCC1), an intrinsic membrane protein expressed by many cell types, is activated by various insults, leading to the formation of cell swelling and brain edema. We previously established that ATX attenuated brain edema and improved neurological outcomes by modulating NKCC1 expression after traumatic brain injury in mice. This paper explored the molecular mechanism of ATX-mediated inhibition of NKCC1 utilizing an in vitro astrocyte stretch injury model.Results: Stretch injury in cultured astrocytes lowered cell viability time-dependently, which was substantially reducing by pretreating with ATX (50 μmol/L). Stretch injury increased Bax level and cleaved caspase-3 activity, and decreased Bcl-2 level and pro-caspase 3 activity, resulting in the apoptosis of astrocytes. Additionally, stretch injury substantially raised the gene and protein expressions of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α and prompted the expression and nuclear translocation of NF-κB. Pretreatment with ATX remarkably prevented the trauma-induced initiation of NF-κB, expressions of pro-inflammatory cytokines, and cell apoptosis. Moreover, stretch injury markedly elevated the gene and protein expression of NKCC1, which was partly blocked by co-treatment with ATX (50 µmol/L) or an NF-κB inhibitor (PDTC, 10 µmol/L). Cleaved caspase-3 activity was partially reduced by PDTC (10 µmol/L) or an NKCC1 inhibitor (bumetanide, 50 µmol/L).Conclusions: ATX attenuates apoptosis after stretch injury in cultured astrocytes by inhibiting NKCC1 expression, and it acts by reducing the expression of NF-κB-mediated pro-inflammatory factors. [ABSTRACT FROM AUTHOR]- Published
- 2017
- Full Text
- View/download PDF
4. Astaxanthin alleviates cerebral edema by modulating NKCC1 and AQP4 expression after traumatic brain injury in mice.
- Author
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Mingkun Zhang, Zhenwen Cui, Hua Cui, Yang Cao, Chunlong Zhong, Yong Wang, Zhang, Mingkun, Cui, Zhenwen, Cui, Hua, Cao, Yang, Zhong, Chunlong, and Wang, Yong
- Subjects
ASTAXANTHIN ,CEREBRAL edema ,BRAIN injuries ,SODIUM-potassium-chloride cotransporters ,AQUAPORINS ,LABORATORY mice ,THERAPEUTICS ,RNA metabolism ,BRAIN metabolism ,ANIMAL experimentation ,BIOLOGICAL models ,BRAIN ,BUMETANIDE ,CAPILLARY permeability ,DRUG design ,DOSE-effect relationship in pharmacology ,CLINICAL drug trials ,MEMBRANE proteins ,MICE ,XANTHOPHYLLS ,NEUROPROTECTIVE agents ,ION transport (Biology) ,PHARMACODYNAMICS - Abstract
Background: Astaxanthin is a carotenoid pigment that possesses potent antioxidative, anti-inflammatory, antitumor, and immunomodulatory activities. Previous studies have demonstrated that astaxanthin displays potential neuroprotective properties for the treatment of central nervous system diseases, such as ischemic brain injury and subarachnoid hemorrhage. This study explored whether astaxanthin is neuroprotective and ameliorates neurological deficits following traumatic brain injury (TBI).Results: Our results showed that, following CCI, treatment with astaxanthin compared to vehicle ameliorated neurologic dysfunctions after day 3 and alleviated cerebral edema and Evans blue extravasation at 24 h (p < 0.05). Astaxanthin treatment decreased AQP4 and NKCC1 mRNA levels in a dose-dependent manner at 24 h. AQP4 and NKCC1 protein expressions in the peri-contusional cortex were significantly reduced by astaxanthin at 24 h (p < 0.05). Furthermore, we also found that bumetanide (BU), an inhibitor of NKCC1, inhibited trauma-induced AQP4 upregulation (p < 0.05).Conclusions: Our data suggest that astaxanthin reduces TBI-related injury in brain tissue by ameliorating AQP4/NKCC1-mediated cerebral edema and that NKCC1 contributes to the upregulation of AQP4 after TBI. [ABSTRACT FROM AUTHOR]- Published
- 2016
- Full Text
- View/download PDF
5. Metabolite differences between glutamate carboxypeptidase II gene knockout mice and their wild-type littermates after traumatic brain injury: a 7-tesla 1H-MRS study.
- Author
-
Wu, Wenbo, Xu, Siyi, Wang, Jialin, Zhang, Kuiming, Zhang, Mingkun, Cao, Yang, Ren, Hongqing, Zheng, Deyou, and Zhong, Chunlong
- Subjects
METABOLITES ,GLUTAMIC acid ,BRAIN injuries ,MAGNETIC resonance imaging ,EDEMA - Abstract
Background: Traumatic brain injury (TBI) is a complex condition and remains a prominent public and medical health issue in individuals of all ages. A rapid increase in extracellular glutamate occurs after TBI, leading to glutamate-induced excitotoxicity, which causes neuronal damage and further functional impairments. Although inhibition of glutamate carboxypeptidase II (GCP II) is considered a potential approach for reducing glutamate-induced excitotoxicity after TBI, further detailed evidence regarding its efficacy is required. Therefore, in this study, we examined the differences in the metabolite status between wild-type (WT) and GCP II gene-knockout (KO) mice after TBI using proton magnetic resonance spectroscopy (1H-MRS) and T2-weighted magnetic resonance (MR) imaging with a 7-tesla imaging system, and brain water-content analysis.Results: Evaluation of glutamate and N-acetylaspartate concentrations revealed a decrease in both levels in the ipsilateral hippocampus at 24 h post-TBI; however, the reduction in glutamate and N-acetylaspartate levels was less marked in GCP II-KO mice than in WT mice (p < 0.05). T2 MR data and brain water-content analysis demonstrated that the extent of cortical edema and brain swelling was less in KO than in WT mice after TBI (p < 0.05).Conclusion: Using two non-invasive methods, 1H-MRS and T2 MR imaging, as well as in vitro brain-water content measurements, we demonstrated that the mechanism underlying the neuroprotective effects of GCP II-KO against brain swelling in TBI involves changes in glutamate and N-acetylaspartate levels. This knowledge may contribute towards the development of therapeutic strategies for TBI. [ABSTRACT FROM AUTHOR]- Published
- 2018
- Full Text
- View/download PDF
6. Astaxanthin protects astrocytes against trauma-induced apoptosis through inhibition of NKCC1 expression via the NF-κB signaling pathway.
- Author
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Zhang M, Cui Z, Cui H, Wang Y, and Zhong C
- Subjects
- Animals, Apoptosis drug effects, Astrocytes pathology, Cells, Cultured, Mice, Mice, Inbred C57BL, NF-kappa B drug effects, NF-kappa B metabolism, Signal Transduction, Solute Carrier Family 12, Member 2 drug effects, Xanthophylls pharmacology, Astrocytes drug effects, Neuroprotective Agents pharmacology, Solute Carrier Family 12, Member 2 biosynthesis
- Abstract
Background: Astaxanthin (ATX) is a carotenoid pigment with pleiotropic pharmacological properties that is seen as a possible drug for treating cerebral ischemic injury and subarachnoid hemorrhage. Na
+ -K+ -2Cl- co-transporter-1 (NKCC1), an intrinsic membrane protein expressed by many cell types, is activated by various insults, leading to the formation of cell swelling and brain edema. We previously established that ATX attenuated brain edema and improved neurological outcomes by modulating NKCC1 expression after traumatic brain injury in mice. This paper explored the molecular mechanism of ATX-mediated inhibition of NKCC1 utilizing an in vitro astrocyte stretch injury model., Results: Stretch injury in cultured astrocytes lowered cell viability time-dependently, which was substantially reducing by pretreating with ATX (50 μmol/L). Stretch injury increased Bax level and cleaved caspase-3 activity, and decreased Bcl-2 level and pro-caspase 3 activity, resulting in the apoptosis of astrocytes. Additionally, stretch injury substantially raised the gene and protein expressions of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α and prompted the expression and nuclear translocation of NF-κB. Pretreatment with ATX remarkably prevented the trauma-induced initiation of NF-κB, expressions of pro-inflammatory cytokines, and cell apoptosis. Moreover, stretch injury markedly elevated the gene and protein expression of NKCC1, which was partly blocked by co-treatment with ATX (50 µmol/L) or an NF-κB inhibitor (PDTC, 10 µmol/L). Cleaved caspase-3 activity was partially reduced by PDTC (10 µmol/L) or an NKCC1 inhibitor (bumetanide, 50 µmol/L)., Conclusions: ATX attenuates apoptosis after stretch injury in cultured astrocytes by inhibiting NKCC1 expression, and it acts by reducing the expression of NF-κB-mediated pro-inflammatory factors.- Published
- 2017
- Full Text
- View/download PDF
7. Astaxanthin alleviates cerebral edema by modulating NKCC1 and AQP4 expression after traumatic brain injury in mice.
- Author
-
Zhang M, Cui Z, Cui H, Cao Y, Zhong C, and Wang Y
- Subjects
- Animals, Brain drug effects, Brain metabolism, Brain pathology, Brain Edema etiology, Brain Edema metabolism, Brain Edema pathology, Brain Injuries, Traumatic complications, Brain Injuries, Traumatic metabolism, Brain Injuries, Traumatic pathology, Bumetanide pharmacology, Capillary Permeability drug effects, Capillary Permeability physiology, Disease Models, Animal, Dose-Response Relationship, Drug, Drug Evaluation, Preclinical, Male, Mice, Inbred C57BL, RNA, Messenger metabolism, Random Allocation, Sodium Potassium Chloride Symporter Inhibitors pharmacology, Xanthophylls pharmacology, Aquaporin 4 metabolism, Brain Edema drug therapy, Brain Injuries, Traumatic drug therapy, Neuroprotective Agents pharmacology, Solute Carrier Family 12, Member 2 metabolism
- Abstract
Background: Astaxanthin is a carotenoid pigment that possesses potent antioxidative, anti-inflammatory, antitumor, and immunomodulatory activities. Previous studies have demonstrated that astaxanthin displays potential neuroprotective properties for the treatment of central nervous system diseases, such as ischemic brain injury and subarachnoid hemorrhage. This study explored whether astaxanthin is neuroprotective and ameliorates neurological deficits following traumatic brain injury (TBI)., Results: Our results showed that, following CCI, treatment with astaxanthin compared to vehicle ameliorated neurologic dysfunctions after day 3 and alleviated cerebral edema and Evans blue extravasation at 24 h (p < 0.05). Astaxanthin treatment decreased AQP4 and NKCC1 mRNA levels in a dose-dependent manner at 24 h. AQP4 and NKCC1 protein expressions in the peri-contusional cortex were significantly reduced by astaxanthin at 24 h (p < 0.05). Furthermore, we also found that bumetanide (BU), an inhibitor of NKCC1, inhibited trauma-induced AQP4 upregulation (p < 0.05)., Conclusions: Our data suggest that astaxanthin reduces TBI-related injury in brain tissue by ameliorating AQP4/NKCC1-mediated cerebral edema and that NKCC1 contributes to the upregulation of AQP4 after TBI.
- Published
- 2016
- Full Text
- View/download PDF
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