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To test the anti\u2010inflammatory and cytoprotective properties, primed\u2010hBMSCs\u2010derived conditioned media (CM) was applied to lipopolysaccharide (LPS)\u2010treated BV2 microglial cells (inflammation model) and BV2 cells exposed to oxygen glucose deprivation (OGD) (hypoxic injury model). The neuroprotective effect was evaluated by assessing neuronal death (using neuron\u2010like cells [NLCs]) following exposure to OGD\/reoxygenation (OGD\/R) in the presence of various CMs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Priming significantly altered hBMSCs' secretion profiles. IL\u20101\u03b1 triggered significant (\n                      <jats:italic>P\u2009&lt;\u20090.05<\/jats:italic>\n                      ) release of inflammatory mediators\/cytokines, notably TNF\u2010\u03b1, ICAM\u20101 and G\u2010CSF. Except for G\u2010SCF, dual\u2010priming did not potentiate their release. While single priming with either IL\u20101\u03b1 or hypoxia\u2010mimetic did not induce remarkable secretion of the neurotrophins \u03b2\u2010NGF and BDNF, the dual\u2010priming caused a potentiated increase (\n                      <jats:italic>P\u2009&lt;\u20090.05<\/jats:italic>\n                      ) in the secretion of these neurotrophins.\n                    <\/jats:p>\n                    <jats:p>\n                      In the LPS model, CM from dual\u2010primed hBMSCs significantly reduced the secretion of pro\u2010inflammatory cytokines, TNF\u2010\u03b1 and IL\u20106. In the OGD\/R model, priming did not significantly influence the marked reduction (\n                      <jats:italic>P\u2009&lt;\u20090.05<\/jats:italic>\n                      ) of pro\u2010inflammatory cytokines IL\u20101\u03b2, IL\u20106 and TNF\u2010\u03b1. Lastly, CMs from primed hBMSCs reduced neuronal cytotoxicity, yet only CM from dual\u2010primed hBMSCs significantly (\n                      <jats:italic>P\u2009&lt;\u20090.05<\/jats:italic>\n                      ) restored metabolic activity in NLCs following OGD\/R.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>These findings highlight dual priming as a promising strategy for optimising MSC\u2010based approaches for hypoxic\u2013ischaemic conditions.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70527","type":"journal-article","created":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T00:56:07Z","timestamp":1781052967000},"page":"5355-5371","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Priming with interleukin\u20101\u03b1 and chemical hypoxia modulates the mesenchymal stem cell secretome to dampen microglial inflammation and promote neuroprotection"],"prefix":"10.1111","volume":"183","author":[{"given":"Maryam Adenike","family":"Salaudeen","sequence":"first","affiliation":[{"name":"Division of Neuroscience, School of Biological Sciences, Faculty of Biology, Medicine, and Health University of Manchester  Manchester UK"},{"name":"Geoffrey Jefferson Brain Research Centre, Manchester Academic Health Science Centre, Northern Care Alliance NHS Foundation Trust University of Manchester  Manchester UK"},{"name":"Department of Pharmacology and Therapeutics Ahmadu Bello University  Zaria Nigeria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stuart M.","family":"Allan","sequence":"additional","affiliation":[{"name":"Division of Neuroscience, School of Biological Sciences, Faculty of Biology, Medicine, and Health University of Manchester  Manchester UK"},{"name":"Geoffrey Jefferson Brain Research Centre, 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