Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/115277
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dc.contributorDepartment of Biomedical Engineeringen_US
dc.contributorMainland Development Officeen_US
dc.contributorDepartment of Applied Physicsen_US
dc.creatorZhang, Qen_US
dc.creatorLi, Cen_US
dc.creatorYin, Ben_US
dc.creatorYan, Jen_US
dc.creatorGu, Yen_US
dc.creatorHuang, Yen_US
dc.creatorChen, Jen_US
dc.creatorLao, Xen_US
dc.creatorHao, Jen_US
dc.creatorYi, Cen_US
dc.creatorZhou, Yen_US
dc.creatorCheung, CWJen_US
dc.creatorWong, SHDen_US
dc.creatorYang, Men_US
dc.date.accessioned2025-09-19T03:23:45Z-
dc.date.available2025-09-19T03:23:45Z-
dc.identifier.urihttp://hdl.handle.net/10397/115277-
dc.language.isoenen_US
dc.publisherKe Ai Publishing Communications Ltden_US
dc.rights© 2024 The Authors. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co. Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).en_US
dc.rightsThe following publication Zhang, Q., Li, C., Yin, B., Yan, J., Gu, Y., Huang, Y., ... & Yang, M. (2024). A biomimetic upconversion nanoreactors for near-infrared driven H2 release to inhibit tauopathy in Alzheimer's disease therapy. Bioactive Materials, 42, 165-177 is available at https://doi.org/10.1016/j.bioactmat.2024.08.029.en_US
dc.subjectArtificial photosynthesisen_US
dc.subjectHydrogen therapyen_US
dc.subjectOxidative stressen_US
dc.subjectTau hyperphosphorylationen_US
dc.subjectAlzheimer's diseaseen_US
dc.titleA biomimetic upconversion nanoreactors for near-infrared driven H₂ release to inhibit tauopathy in Alzheimer's disease therapyen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage165en_US
dc.identifier.epage177en_US
dc.identifier.volume42en_US
dc.identifier.doi10.1016/j.bioactmat.2024.08.029en_US
dcterms.abstractAbnormal hyperphosphorylation of tau protein is a principal pathological hallmark in the onset of neurodegenerative disorders, such as Alzheimer's disease (AD), which can be induced by an excess of reactive oxygen species (ROS). As an antioxidant, hydrogen gas (H<inf>2</inf>) has the potential to mitigate AD by scavenging highly harmful ROS such as •OH. However, conventional administration methods of H<inf>2</inf> face significant challenges in controlling H<inf>2</inf> release on demand and fail to achieve effective accumulation at lesion sites. Herein, we report artificial nanoreactors that mimic natural photosynthesis to realize near-infrared (NIR) light-driven photocatalytic H<inf>2</inf> evolution in situ. The nanoreactors are constructed by biocompatible crosslinked vesicles (CVs) encapsulating ascorbic acid and two photosensitizers, chlorophyll a (Chla) and indoline dye (Ind). In addition, platinum nanoparticles (Pt NPs) serve as photocatalysts and upconversion nanoparticles (UCNP) act as light-harvesting antennas in the nanoreacting system, and both attach to the surface of CVs. Under NIR irradiation, the nanoreactors release H<inf>2</inf> in situ to scavenge local excess ROS and attenuate tau hyperphosphorylation in the AD mice model. Such NIR-triggered nanoreactors provide a proof-of-concept design for the great potential of hydrogen therapy against AD.en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationBioactive materials, Dec. 2024, v. 42, p. 165-177en_US
dcterms.isPartOfBioactive materialsen_US
dcterms.issued2024-12-
dc.identifier.scopus2-s2.0-85202582671-
dc.identifier.eissn2452-199Xen_US
dc.description.validate202509 bchyen_US
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberCDCF_2024-2025-
dc.description.fundingSourceRGCen_US
dc.description.fundingSourceOthersen_US
dc.description.fundingTextFunding text 1: In addition, we evaluated the ROS levels in the cerebral areas using DCFH-DA probe. Strikingly, ROS levels of the hippocampus and cortex in the AD model were amplified by 4.6 and 6.4 folds compared to the wild-type counterparts (Fig. 7a and c). Administration with CVs@Pt@UCNP and (Chla + Ind)@NR without NIR laser did not affect ROS level (Fig. 7a). An astounding ROS scavenging occurred in groups treated with NRs in the presence of NIR irradiation with the following efficiency order: (Chla + Ind)@NR > Chla@NR \u2248 Ind@NR (Fig. 7c). This trend of ROS removal for the in vivo results is consistent with those in the in vitro study (Fig. 3c\u2013e). Moreover, we conducted an immunofluorescence assay to evaluate the expression of p-tau in the brain area. The results demonstrated nearly undetectable p-tau in wild-type mice. However, the AD model showed intense punctate staining of p-tau, with the hippocampal and cortical regions showing 4.1-fold and 2.6-fold higher fluorescent intensity than that of the wild type, respectively (Fig. 7b and d). Obviously, the microinjection of our NRs (Chla@NR, Ind@NR, and (Chla + Ind)@NR) with subsequent NIR laser irradiation significantly mitigated p-tau expression. Specifically, fluorescent signals of p-tau in the hippocampus and cortex of the NIR-triggered (Chla + Ind)@NR group were only \u223C1.8 and \u223C1.6 times those in wild-type mice (Fig. 7b and d). Taken together, these histological analyses strongly support that our NRs effectively neutralize ROS overproduction in neuronal cells under NIR irradiation to prevent tau hyperphosphorylation in AD pathology.This work was supported by the Shenzhen Science and Technology Program-Basic Research Scheme (JCYJ20220531090808020), the Research Grants Council (RGC) of Hong Kong Collaborative Research Grant (C5005-23W and C5078-21E), the Research Grants Council (RGC) of Hong Kong General Research Grant (PolyU 15217621 and PolyU 15216622), the Guangdong-Hong Kong Technology Cooperation Funding Scheme (GHP/032/20SZ and SGDX20201103095404018), the Hong Kong Polytechnic University Shenzhen Institute Bai Cheng Bai Yuan Fund (I2022A002), PolyU Internal Fund (1-YWB4, 1-WZ4E, 1-CD8M, 1-WZ4E, 1-CEB1, 1-YWDU, 1-CE2J and 1-W02C). We also would like to acknowledge the funding from the Laboratory for Marine Drugs and Bioproducts, Qingdao Marine Science and Technology Center (No.: LMDBCXRC202401 and LMDBCXRC202402), Shandong Provincial Overseas Excellent Young Scholar Program (2024HWYQ-042 and 2024HWYQ-043) and Taishan Scholar Youth Expert Program of Shandong Province (tsqn202306102 and tsqn202312105) supporting this work. This work was also supported by the University Research Facility in Life Sciences of the Hong Kong Polytechnic University.; Funding text 2: This work was supported by the Shenzhen Science and Technology Program-Basic Research Scheme (JCYJ20220531090808020), the Research Grants Council (RGC) of Hong Kong Collaborative Research Grant (C5005-23W and C5078-21E), the Research Grants Council (RGC) of Hong Kong General Research Grant (PolyU 15217621 and PolyU 15216622), the Guangdong-Hong Kong Technology Cooperation Funding Scheme (GHP/032/20SZ and SGDX20201103095404018), the Hong Kong Polytechnic University Shenzhen Institute Bai Cheng Bai Yuan Fund (I2022A002), PolyU Internal Fund (1-YWB4, 1-WZ4E, 1-CD8M, 1-WZ4E, 1-CEB1, 1-YWDU, 1-CE2J and 1-W02C). We also would like to acknowledge the funding from the Laboratory for Marine Drugs and Bioproducts, Qingdao Marine Science and Technology Center (No.: LMDBCXRC202401 and LMDBCXRC202402), Shandong Provincial Overseas Excellent Young Scholar Program (2024HWYQ-042 and 2024HWYQ-043) and Taishan Scholar Youth Expert Program of Shandong Province (tsqn202306102 and tsqn202312105) supporting this work. This work was also supported by the University Research Facility in Life Sciences of the Hong Kong Polytechnic University.en_US
dc.description.pubStatusPublisheden_US
dc.description.oaCategoryCCen_US
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