The Journal of Practical Medicine >
Effect of M1 microglial polarization on secondary damage in the thalamus after cerebral cortical infarction
Received date: 2024-07-12
Online published: 2024-11-25
Objective To explore the effects of M1 polarization of microglia on secondary damage in the thalamus after cerebral cortical infarction. Methods A focal cortical infarct model of adult male SD rats was prepared using eletrocoagulation and randomized into Sham and model groups at different time points 1 ~ 4 weeks after surgery. Based on the assessment of neurofunctional changes in each group of rats， immunohistochemistry was used to observe the number and morphology of NeuN， GFAP and Iba-1 positive cells in （Ventral posterior nucleus of thalamus， VPN） of the ipsilateral thalamus after distal middle cerebral artery occlusion （dMCAO）. Immunofurescence was used to detect the number and morphology of M1 microglia marker （Iba-1+/CD68+ cells） and M2 microglia marker （Iba-1+/CD206+ cells） in VPN of the ipsilateral thalamus after dMCAO. Western blot was used to detect the expression levels of IL-1β， TNF-α， IL-10 and Arg-1 in VPN of the ipsilateral thalamus after dMCAO. Results The results of immunohistochemistry showed a significant decrease in NeuN positive cells and an increase in the density of GFAP and Iba-1 in the ipsilateral VPN of rats after dMCAO when compared with Sham group （P < 0.001）. Compared with sham group， the protein levels of TNFα and IL-1β were elevated in the ipsilateral VPN elevated （P < 0.05）. In addition， the model group rats exhibited higher Bederson scores， beam-walking test and adhesive removal test scores after dMCAO compared with Sham group （P < 0.05）. The numbers of M1 microglia marker （Iba-1+/CD68+ cells） were significantly increased when compared with M2 microglia marker （Iba-1+/CD206+ cells） in ipsilateral VPN of rats after dMCAO. Conclusion M1 polarization of microglia may play an essential role in secondary damage of thalamus after cerebral cortical infarction.
Zhe SHI , Xialin ZUO , Linhui PENG , Zhiwei LU , Kongping. LI . Effect of M1 microglial polarization on secondary damage in the thalamus after cerebral cortical infarction[J]. The Journal of Practical Medicine, 2024 , 40(22) : 3138 -3145 . DOI: 10.3969/j.issn.1006-5725.2024.22.004
| 1 | CAO Z， HARVEY S S， BLISS T M， et al. Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke ［J］. Front Neurol， 2020， 11： 236. doi:10.3389/fneur.2020.00236 |
| 2 | ZHOU K， TAN Y， ZHANG G， et al. Loss of SARM1 ameliorates secondary thalamic neurodegeneration after cerebral infarction ［J］. J Cereb Blood Flow Metab. 2024， 44（2）： 224-238. doi:10.1177/0271678x231210694 |
| 3 | 李虹莹，沈缘，吴巧凤，等. 小胶质细胞极化信号通路在神经炎症中的研究进展 ［J］. 实用医学杂志， 2022， 38 （14）： 1838-1846. doi:10.3969/j.issn.1006?5725.2022.14.024 |
| 4 | FAN P L， WANG S S， CHU S F， et al. Time-dependent dual effect of microglia in ischemic stroke ［J］. Neurochem Int， 2023， 169：105584. doi:10.1016/j.neuint.2023.105584 |
| 5 | DARWISH S F， ELBADRY A M M， ELBOKHOMY A S， et al. The dual face of microglia （M1/M2） as a potential target in the protective effect of nutraceuticals against neurodegenerative diseases ［J］. Front Aging， 2023， 4：1231706. doi:10.3389/fragi.2023.1231706 |
| 6 | SURUGIU R， CATALIN B， DUMBRAVA D， et al. Intracortical Administration of the Complement C3 Receptor Antagonist Trifluoroacetate Modulates Microglia Reaction after Brain Injury ［J］. Neural Plast， 2019， 2019：1071036. doi:10.1155/2019/1071036 |
| 7 | LI J， WANG H， DU C， et al. hUC-MSCs ameliorated CUMS-induced depression by modulating complement C3 signaling-mediated microglial polarization during astrocyte-microglia crosstalk ［J］. Brain Res Bull， 2020， 163：109-119. doi:10.1016/j.brainresbull.2020.07.004 |
| 8 | DATTA A， SARMAH D， KALIA K， et al. Advances in Studies on Stroke-Induced Secondary Neurodegeneration （SND） and Its Treatment ［J］. Curr Top Med Chem， 2020， 20（13）：1154-1168. doi:10.2174/1568026620666200416090820 |
| 9 | LI K， PENG L， XING Q， et al. Transplantation of hESCs-Derived Neural Progenitor Cells Alleviates Secondary Damage of Thalamus After Focal Cerebral Infarction in Rats ［J］. Stem Cells Transl Med， 2023， 12（8）：553-568. doi:10.1093/stcltm/szad037 |
| 10 | JIANG Z， WEI J， LIANG J， et al. Dl-3-n-Butylphthalide Alleviates Secondary Brain Damage and Improves Working Memory After Stroke in Cynomolgus Monkeys ［J］. Stroke，2024， 55（3）：725-734. doi:10.1161/strokeaha.123.045037 |
| 11 | KANEMITSU H， NAKAGOMI T， TAMURA A， et al. Differences in the extent of primary ischemic damage between middle cerebral artery coagulation and intraluminal occlusion models ［J］. J Cereb Blood Flow Metab， 2002， （10）：1196-1204. doi:10.1097/01.wcb.0000037992.07114.95 |
| 12 | ZENG L， HU S， ZENG L， et al. Animal Models of Ischemic Stroke with Different Forms of Middle Cerebral Artery Occlusion ［J］. Brain Sci，2023， 13（7）：1007. doi:10.3390/brainsci13071007 |
| 13 | 刘毅， 孙邈， 吉训明， 等. 丘脑供血及丘脑缺血性卒中临床表现［J］. 中国现代神经疾病杂志， 2018，18（12）：902-905. |
| 14 | ONG L K. Beyond the Primary Infarction： Focus on Mechanisms Related to Secondary Neurodegeneration after Stroke［J］. Int J Mol Sci，2022， 23（24）：16024. doi:10.3390/ijms232416024 |
| 15 | BRUNELLI S， GIANNELLA E， BIZZAGLIA M， et al. Secondary neurodegeneration following Stroke： What can blood biomarkers tell us？ ［J］. Front Neurol，2023， 14：1198216. doi:10.3389/fneur.2023.1198216 |
| 16 | STUCKEY S M， ONG L K， COLLINS-PRAINO L E， et al. Neuroinflammation as a Key Driver of Secondary Neurodegeneration Following Stroke？ ［J］. Int J Mol Sci，2021， 22（23）：13101. doi:10.3390/ijms222313101 |
| 17 | PENG L， LI K， LI D， et al. The p75 neurotrophin receptor attenuates secondary thalamic damage after cortical infarction by promoting angiogenesis ［J］. CNS Neurosci Ther，2024， 30（7）：e14875. doi:10.1111/cns.14875 |
| 18 | DUAN M， XU Y， LI Y， et al. Targeting brain-peripheral immune responses for secondary brain injury after ischemic and hemorrhagic stroke ［J］. J Neuroinflammation，2024， 21（1）：102. doi:10.1186/s12974-024-03101-y |
| 19 | KIM G S， HARMON E， GUTIERREZ M， et al. Single-cell analysis identifies Ifi27l2a as a novel gene regulator of microglial inflammation in the context of aging and stroke ［J］. Res Sq ［Preprint］，2023， rs.3.rs-2557290. |
| 20 | NECULA D， CHO F S， HE A， et al. Secondary thalamic neuroinflammation after focal cortical stroke and traumatic injury mirrors corticothalamic functional connectivity ［J］. J Comp Neurol，2022， 530（7）：998-1019. doi:10.1002/cne.25259 |
| 21 | 王方明，尚文璇，张靖雯，等. 自噬调控小胶质细胞极化在缺血性脑卒中的研究进展 ［J］. 实用医学杂志，2024， 40（9）： 1324-1330. |
| 22 | D'ANMA L， SEARLE G， HARVEY K，et al. Time course of neuroinflammation after human stroke-A pilot study using co-registered PET and MRI ［J］. BMC Neurol，2023， 23（1）：193. doi:10.1186/s12883-023-03178-7 |
| 23 | ANTTILA J E， ALBERT K， WIRES E S， et al. Post-stroke Intranasal （+）-Naloxone Delivery Reduces Microglial Activation and Improves Behavioral Recovery from Ischemic Injury ［J］. eNeuro， 2018， 5（2）：ENEURO.0395-17.2018. doi:10.1523/eneuro.0395-17.2018 |
| 24 | SHUI X， CHEN J， FU Z， et al. Microglia in Ischemic Stroke： Pathogenesis Insights and Therapeutic Challenges ［J］. J Inflamm Res， 2024， 17： 3335-3352. doi:10.2147/jir.s461795 |
| 25 | WANG H， LI X， WANG Q， et al. TREM2， microglial and ischemic stroke ［J］. J Neuroimmunol， 2023， 381：578108. doi:10.1016/j.jneuroim.2023.578108 |
| 26 | BERNIS M E， SCHLEEHUBER Y， ZWEYER M， et al. Temporal Characterization of Microglia-Associated Pro- and Anti-Inflammatory Genes in a Neonatal Inflammation-Sensitized Hypoxic-Ischemic Brain Injury Model ［J］. Oxid Med Cell Longev， 2022， 2022：2479626. doi:10.1155/2022/2479626 |
| 27 | CAO Z， HARVEY S S， CHIANG T， et al. Unique Subtype of Microglia in Degenerative Thalamus After Cortical Stroke ［J］. Stroke， 2021， 52（2）：687-698. doi:10.1161/strokeaha.120.032402 |
| 28 | ZHENG Y， HU Y， YAN F， et al. Dihydroergotamine protects against ischemic stroke by modulating microglial/macrophage polarization and inhibiting inflammation in mice ［J］. Neurol Res，2024， 46（4）：367-377. doi:10.1080/01616412.2024.2328481 |
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