{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,22]],"date-time":"2026-04-22T10:04:49Z","timestamp":1776852289040,"version":"3.51.2"},"reference-count":32,"publisher":"BMJ","issue":"5","funder":[{"name":"Chongqing Outstanding Scientists Project","award":["2019"],"award-info":[{"award-number":["2019"]}]},{"name":"Beijing Municipal Public Welfare Development and Reform Pilot Project for Medical Research Institutes","award":["JYY2023-6"],"award-info":[{"award-number":["JYY2023-6"]}]},{"name":"Beijing Municipal Public Welfare Development and Reform Pilot Project for Medical Research Institutes","award":["PWD&RPP-MRI"],"award-info":[{"award-number":["PWD&RPP-MRI"]}]},{"name":"Chongqing Chief Medical Scientist Project","award":["2018"],"award-info":[{"award-number":["2018"]}]},{"name":"Chongqing Science and Technology Bureau Mountaineering Project","award":["cyyy-xkdfjh-cgzh-202302"],"award-info":[{"award-number":["cyyy-xkdfjh-cgzh-202302"]}]},{"name":"Chongqing Science and Technology Bureau Mountaineering Project","award":["cyyy-xkdfjh-jcyj-202301"],"award-info":[{"award-number":["cyyy-xkdfjh-jcyj-202301"]}]},{"name":"Chongqing Science and Technology Bureau Mountaineering Project","award":["cyyy-xkdfjh-lcyj-202303"],"award-info":[{"award-number":["cyyy-xkdfjh-lcyj-202303"]}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation Project of China","doi-asserted-by":"crossref","award":["82230032"],"award-info":[{"award-number":["82230032"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation Project of China","doi-asserted-by":"crossref","award":["82271078"],"award-info":[{"award-number":["82271078"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Youth Beijing Scholar","award":["No.076"],"award-info":[{"award-number":["No.076"]}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["Br J Ophthalmol"],"accepted":{"date-parts":[[2025,7,29]]},"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Retinopathy of prematurity (ROP), an oxygen-induced retinopathy (OIR), triggers a series of vascular lesions and inflammatory responses and results in visual impairment or even blindness. Triptolide (TP) possesses many pharmacological properties, including immunosuppressive and anti-tumour effects. However, the effects of TP on ROP and its underlying mechanisms remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>To investigate whether TP could inhibit the progression of OIR and to elucidate its underlying mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The 7-day-old mice (P7) were kept in a 75% hyperoxia incubator for 5\u2009days to induce an OIR model, followed by TP treatment for 5\u2009days. Biomedical analysis and histopathological examinations of harvested retinas were conducted to explore the effect of TP. Furthermore, the impact of TP on retinal neovascularisation and microglial activation was validated using human umbilical vein endothelial cells (HUVECs) and human microglial clone 3 cells (HMC3s).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>TP treatment could significantly alleviate retinal pathological neovascularisation by inhibiting microglial activation. It downregulated the elevated levels of inflammatory cytokines (inducible nitric oxide synthase, tumour necrosis factor-\u03b1, Cox2 and interleukin (IL)-1\u03b2) and angiogenesis-related factors (hypoxia-inducible factor-1\u03b1, matrix metalloproteinase-2 and vascular endothelial growth factor-A) in OIR retinas and hypoxic HMC3s. HUVECs\u2019 migration, proliferation and tube-forming capacities were also markedly suppressed under TP treatment. Further analysis suggested that TP exerted its anti-angiogenic effect in a way similar to NF-\u03baB inhibitor (BAY117082).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>TP alleviates pathological neovascularisation in OIR, potentially through the inhibition of inflammation mediated by NF-\u03baB pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/bjo-2024-326932","type":"journal-article","created":{"date-parts":[[2025,9,8]],"date-time":"2025-09-08T17:24:10Z","timestamp":1757352250000},"page":"527-535","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Triptolide alleviates pathological neovascularisation in oxygen-induced retinopathy via inhibiting the inflammation mediated by NF-\u03baB 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