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The latter could strongly stimulate MiR\u2010155 that contributes to neurodegeneration and Alzheimer's disease (AD). miR\u2010155 could repress the expression of inositol 5\u2010phosphatase\u20101 (SHIP\u20101) leading eventually to activation of Akt kinase and neurofibrillary development in AD. The current study was conducted to evaluate the role of miR\u2010155 in a rat model of lipopolysaccharide (LPS)\u2010induced AD and to investigate the effect of using MVs and H<jats:sub>2<\/jats:sub>S that were given either separately or combined in regulating pro\u2010inflammatory signaling. Thirty female Wistar albino rats aged 6 months to 1 year were equally divided into five\u00a0groups; control group, LPS\u2010induced AD group, LPS\u2009+\u2009MVs group, LPS\u2009+\u2009NaHS group, and LPS\u2009+\u2009MVs and NaHS group. The increased miR\u2010155 level was associated with decreased SHIP\u20101 level and positively correlated with TNF\u2010\u03b1. In addition, treatment with MVs and\/or NaHS resulted in attenuation of inflammation, decreasing miR\u2010155, pAkt levels, and downregulation of apoptosis along with improvement of the hippocampal and cortical histopathological alterations. LPS enhanced production of malondialdehyde (MDA) and reduced glutathione (GSH) levels indicating oxidative stress\u2010induced neural damage, whereas MVs and NaHS could mitigate oxidative damage and accelerate antioxidant capacity via increasing catalase enzyme. In conclusion, downregulation of TNF\u2010\u03b1, miR\u2010155, and pAkt and increased SHIP\u20101 could improve the neuro\u2010inflammatory state and cognitive function of LPS\u2010induced Alzheimer's disease.<\/jats:p>","DOI":"10.1002\/jcp.30283","type":"journal-article","created":{"date-parts":[[2021,1,23]],"date-time":"2021-01-23T04:02:04Z","timestamp":1611374524000},"page":"5994-6010","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Hydrogen sulfide and mesenchymal stem cells\u2010extracted microvesicles attenuate LPS\u2010induced Alzheimer's disease"],"prefix":"10.1002","volume":"236","author":[{"given":"Basma E.","family":"Aboulhoda","sequence":"first","affiliation":[{"name":"Department of Anatomy and Embryology, Faculty of Medicine Cairo University  Giza Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laila A.","family":"Rashed","sequence":"additional","affiliation":[{"name":"Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine Cairo University  Giza Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hoda","family":"Ahmed","sequence":"additional","affiliation":[{"name":"Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine Cairo University  Giza Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eman M. 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