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您的检索式：作者名="Mengye Zhu"
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| 1 | Iron oxide nanoparticles promote vascular endothelial cells survival from oxidative stress by enhancement of autophagy显示文摘Dextran-coated superparamagnetic iron oxide nanoparticles(Dex-SPIONs)are excellent magnetic resonance imaging contrast agents for disease diagnosis and therapy.They can be delivered to target tissues mainly though vascular endothelium cells,which are major targets of oxidative stress.In cardiovascular cells,autophagy serves primarily on a pro-survival approach that protects the cells from oxidative stress even some autophagy inducers have been developed for adjuvant therapy of cardiovascular disorders.Our study demonstrated that the nanoparticles could be taken up by human umbilical vein endothelial cells(HUVECs)without causing obvious cytotoxicity but triggering autophagy.Furthermore,our results revealed that Dex-SPIONs could enhance HUVECs survival and reverse the reduction of nitric oxide secretion under the condition of H2O2 damage.However,these effects could be diminished by the autophagy inhibitor.In particular,we discovered that Dex-SPIONs evoked autophagy in HUVECs by reducing the phosphorylation of PRAS40,an upstream regulator of autophagy initiation.These results suggested that Dex-SPIONs functions as an autophagic-related antioxidant in HUVECs which may be utilized as an adjuvant therapy to cardiovascular disease associated with oxidative stress. | Jimei Duan Jiuju Du Rongrong Jin Wencheng Zhu Li Liu Li Yang Mengye Li Qiyong Gong Bin Song James MAnderson and Hua Ai | 2019 | Regenerative Biomaterials2019，6，4： | 2 |
| 2 | Thalamocortical Circuit Controls Neuropathic Pain via Up-regulation of HCN2 in the Ventral Posterolateral显示文摘The thalamocortical(TC)circuit is closely asso-ciated with pain processing.The hyperpolarization-activated cyclic nucleotide-gated(HCN)2 channel is predominantly expressed in the ventral posterolateral thalamus(VPL)that has been shown to mediate neuropathic pain.However,the role of VPL HCN2 in modulating TC circuit activity is largely unknown.Here,by using optogenetics,neuronal trac-ing,electrophysiological recordings,and virus knockdown strategies,we showed that the activation of VPL TC neurons potentiates excitatory synaptic transmission to the hindlimb region of the primary somatosensory cortex(S1HL)as well as mechanical hypersensitivity following spared nerve injury(SNI)-induced neuropathic pain in mice.Either pharmaco-logical blockade or virus knockdown of HCN2(shRNA-Hcn2)in the VPL was sufficient to alleviate SNI-induced hyperalgesia.Moreover,shRNA-Hcn2 decreased the excitability of TC neurons and synaptic transmission of the VPL-S1HL circuit.Together,our studies provide a novel mechanism by which HCN2 enhances the excitability of the TC circuit to facilitate neuropathic pain. | Yi Yan Mengye Zhu Xuezhong Cao Gang Xu Wei Shen Fan Li Jinjin Zhang Lingyun Luo Xuexue Zhang Daying Zhang Tao Liu | 2023 | Neuroscience Bulletin2023，39，5： | 0 |
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