Background:Ischemic stroke is characterized by permanent or transient obstruction of blood flow,leading to a growing risk factor and health burden.Tianmagouteng yin(TMG)is commonly used in Chinese medicine to treat ce...Background:Ischemic stroke is characterized by permanent or transient obstruction of blood flow,leading to a growing risk factor and health burden.Tianmagouteng yin(TMG)is commonly used in Chinese medicine to treat cerebral ischemia.The aim of this study was to investigate the neuroprotective effects of TMG against ischemic stroke.Methods:Either permanent middle cerebral artery occlusion(pMCAO)or sham operation was performed on anesthetized Wistar male rats(n=36).Results:Results demonstrated that TMG administration reduced the infarction volume and mitigated the neurobehavioral deficits.Hematoxylin and eosin(HE)staining and Prussian blue staining revealed that TMG attenuated tissue disruption and microbleeds in hippocampus tissues.In addition,TMG down-regulated the receptor of advanced glycation end products(RAGE)and p-JAK2.It also inhibited the concentrations of advanced glycation end products(AGEs),ferritin,malondialdehyde(MDA),and reactive oxygen species(ROS).Conclusion:As repetitive clinical trials of neuroprotectants targeting stroke have failed previously,our results suggested that the natural product,TMG,can probably help in the vicious cycles of ischemic stroke pathology.展开更多
This study aimed to assess the role of microRNAs(miRNAs)in regulating monocarboxylate transporter-1(MCT1)expression in rat brain after permanent focal cerebral ischemia to identify a new target for early treatment of ...This study aimed to assess the role of microRNAs(miRNAs)in regulating monocarboxylate transporter-1(MCT1)expression in rat brain after permanent focal cerebral ischemia to identify a new target for early treatment of cerebral ischemia.Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion(pMCAO)in rats.Morphology and protein expression levels of MCT1 were assessed by immunofluorescence and Western blotting.Using bioinformatics and double luciferase reporter assays,rno-miR-124-3p was selected as a direct target for rat MCT1.Expression of rno-miR-124-3p after pMCAO was detected.Then,rats were treated with rno-miR-124-3p agomir via lateral ventricle injection,and after 6 h or 24 h ischemia,rno-miR-124-3p expression and gene and protein expression of MCT-1 were detected by qRT-PCR and Western blotting.Brain infarction was identified by 2,3,5-triphenyltetrazolium chloride(TTC)staining.Results showed that pMCAO induced brain infarction and increased the expression of MCT1.The levels of rno-miR-124-3p after pMCAO were in contrast to those of MCT1 protein in ischemic region,while declined after 3,6 and 12 h of pMCAO in ischemic penumbra.After administration of rno-miR-124-3p agomir,MCT1 mRNA and protein levels were increased after 6 h of pMCAO,while decreased after 24 h of pMCAO.Meanwhile,rno-miR-124-3p levels increased after both times.TTC staining showed treatment with rno-miR-124-3p agomir reduced brain infarction.The role of rno-miR-124-3p in regulating MCT1 was as a positive regulator after 6 h of pMCAO,while a negative regulator after 24 h of pMCAO,however,both activities had protective effects against cerebral ischemia.展开更多
基金Zhejiang TCM Science and Technology Program[Grant Number 2021ZA050].
文摘Background:Ischemic stroke is characterized by permanent or transient obstruction of blood flow,leading to a growing risk factor and health burden.Tianmagouteng yin(TMG)is commonly used in Chinese medicine to treat cerebral ischemia.The aim of this study was to investigate the neuroprotective effects of TMG against ischemic stroke.Methods:Either permanent middle cerebral artery occlusion(pMCAO)or sham operation was performed on anesthetized Wistar male rats(n=36).Results:Results demonstrated that TMG administration reduced the infarction volume and mitigated the neurobehavioral deficits.Hematoxylin and eosin(HE)staining and Prussian blue staining revealed that TMG attenuated tissue disruption and microbleeds in hippocampus tissues.In addition,TMG down-regulated the receptor of advanced glycation end products(RAGE)and p-JAK2.It also inhibited the concentrations of advanced glycation end products(AGEs),ferritin,malondialdehyde(MDA),and reactive oxygen species(ROS).Conclusion:As repetitive clinical trials of neuroprotectants targeting stroke have failed previously,our results suggested that the natural product,TMG,can probably help in the vicious cycles of ischemic stroke pathology.
文摘This study aimed to assess the role of microRNAs(miRNAs)in regulating monocarboxylate transporter-1(MCT1)expression in rat brain after permanent focal cerebral ischemia to identify a new target for early treatment of cerebral ischemia.Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion(pMCAO)in rats.Morphology and protein expression levels of MCT1 were assessed by immunofluorescence and Western blotting.Using bioinformatics and double luciferase reporter assays,rno-miR-124-3p was selected as a direct target for rat MCT1.Expression of rno-miR-124-3p after pMCAO was detected.Then,rats were treated with rno-miR-124-3p agomir via lateral ventricle injection,and after 6 h or 24 h ischemia,rno-miR-124-3p expression and gene and protein expression of MCT-1 were detected by qRT-PCR and Western blotting.Brain infarction was identified by 2,3,5-triphenyltetrazolium chloride(TTC)staining.Results showed that pMCAO induced brain infarction and increased the expression of MCT1.The levels of rno-miR-124-3p after pMCAO were in contrast to those of MCT1 protein in ischemic region,while declined after 3,6 and 12 h of pMCAO in ischemic penumbra.After administration of rno-miR-124-3p agomir,MCT1 mRNA and protein levels were increased after 6 h of pMCAO,while decreased after 24 h of pMCAO.Meanwhile,rno-miR-124-3p levels increased after both times.TTC staining showed treatment with rno-miR-124-3p agomir reduced brain infarction.The role of rno-miR-124-3p in regulating MCT1 was as a positive regulator after 6 h of pMCAO,while a negative regulator after 24 h of pMCAO,however,both activities had protective effects against cerebral ischemia.
