File Download
There are no files associated with this item.
Supplementary
-
Citations:
- Appears in Collections:
Conference Paper: Inhibition of C-X-C Motif Chemokine Receptor 3 (CXCR3) improves the outcomes of intracerebral hemorrhage
Title | Inhibition of C-X-C Motif Chemokine Receptor 3 (CXCR3) improves the outcomes of intracerebral hemorrhage |
---|---|
Authors | |
Issue Date | 2021 |
Publisher | The Hong Kong Neurosurgical Society. |
Citation | 28th Annual Scientific Meeting of The Hong Kong Neurosurgical Society: Updates on Traumatic Brain Injury and Neurocritical Care, Virtual Meeting, Hong Kong, 26-27 November 2021 How to Cite? |
Abstract | Objective: To examine the effects of inhibition of CXCR3, a chemokine receptor, on the outcomes of experimental intracerebral hemorrhage (ICH) and to explore the potential underlying mechanism.
Method: Wild-type C57BL/6N and CXCR3 Knock-Out mice were used in this study. Experimental ICH was induced via intra-striatal injection of 0.04U Type IV collagenase in 0.5ul of 0.9% normal saline. The cylinder test, rotarod test and grid walking test were used to assess motor outcomes. Demyelination was examined by transmission electron microscopy and immunofluorescence staining. Real-time quantitative polymerase chain reaction was used to quantify the relative mRNA expression levels of CXCR3 and pro-inflammatory markers. The cell types that expressed CXCR3 and the changes in the percentages of various cell populations in brain and blood were detected by flow cytometry.
Result: CXCR3 Knock-Out mice had better motor functions especially in the first week after ICH. The degree of demyelination of the CXCR3 Knock-out mice was less severe compared to that of the Wild-Type mice. The relative expression levels of several pro-inflammatory markers are under investigation. CXCR3 mRNA expression was upregulated in the perihaematomal area but not in the contralateral hemisphere. A subpopulation of T cells was the main cell type that carried CXCR3. Preliminary result showed that CXCR3 expression was also upregulated in a T cell subpopulation in the peripheral blood in addition to its upregulation in the brain post-ICH.
Conclusion: The inhibition of CXCR3 improves outcomes of ICH in mice potentially via the reduction in neuroinflammation. |
Description | Oral Presentation - Free Paper II-Vascular |
Persistent Identifier | http://hdl.handle.net/10722/309045 |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | NG, CKA | - |
dc.contributor.author | LIU, JXC | - |
dc.contributor.author | Kiang, MYK | - |
dc.contributor.author | Zhu, ZYJ | - |
dc.contributor.author | Chau, KCW | - |
dc.contributor.author | Lam, TL | - |
dc.contributor.author | Leung, GKK | - |
dc.date.accessioned | 2021-12-14T01:39:51Z | - |
dc.date.available | 2021-12-14T01:39:51Z | - |
dc.date.issued | 2021 | - |
dc.identifier.citation | 28th Annual Scientific Meeting of The Hong Kong Neurosurgical Society: Updates on Traumatic Brain Injury and Neurocritical Care, Virtual Meeting, Hong Kong, 26-27 November 2021 | - |
dc.identifier.uri | http://hdl.handle.net/10722/309045 | - |
dc.description | Oral Presentation - Free Paper II-Vascular | - |
dc.description.abstract | Objective: To examine the effects of inhibition of CXCR3, a chemokine receptor, on the outcomes of experimental intracerebral hemorrhage (ICH) and to explore the potential underlying mechanism. Method: Wild-type C57BL/6N and CXCR3 Knock-Out mice were used in this study. Experimental ICH was induced via intra-striatal injection of 0.04U Type IV collagenase in 0.5ul of 0.9% normal saline. The cylinder test, rotarod test and grid walking test were used to assess motor outcomes. Demyelination was examined by transmission electron microscopy and immunofluorescence staining. Real-time quantitative polymerase chain reaction was used to quantify the relative mRNA expression levels of CXCR3 and pro-inflammatory markers. The cell types that expressed CXCR3 and the changes in the percentages of various cell populations in brain and blood were detected by flow cytometry. Result: CXCR3 Knock-Out mice had better motor functions especially in the first week after ICH. The degree of demyelination of the CXCR3 Knock-out mice was less severe compared to that of the Wild-Type mice. The relative expression levels of several pro-inflammatory markers are under investigation. CXCR3 mRNA expression was upregulated in the perihaematomal area but not in the contralateral hemisphere. A subpopulation of T cells was the main cell type that carried CXCR3. Preliminary result showed that CXCR3 expression was also upregulated in a T cell subpopulation in the peripheral blood in addition to its upregulation in the brain post-ICH. Conclusion: The inhibition of CXCR3 improves outcomes of ICH in mice potentially via the reduction in neuroinflammation. | - |
dc.language | eng | - |
dc.publisher | The Hong Kong Neurosurgical Society. | - |
dc.relation.ispartof | The Hong Kong Neurosurgical Society 28th Annual Scientific Meeting (Virtual), 2021 | - |
dc.title | Inhibition of C-X-C Motif Chemokine Receptor 3 (CXCR3) improves the outcomes of intracerebral hemorrhage | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Kiang, MYK: mykiang@hku.hk | - |
dc.identifier.email | Zhu, ZYJ: jzhu2020@hku.hk | - |
dc.identifier.email | Leung, GKK: gkkleung@hku.hk | - |
dc.identifier.authority | Leung, GKK=rp00522 | - |
dc.identifier.hkuros | 331056 | - |
dc.publisher.place | Hong Kong | - |