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Injection of 3-nitropropionic acid (3-NP) is a widely used experimental model for induction of HD. The current study aimed to inspect the potential neuroprotective properties of azilsartan (Azil), an angiotensin II type 1 receptor blocker (ATR1), in 3-NP-induced striatal neurotoxicity in rats. Rats were randomly allocated into five groups and treated for 14 days as follows: group I received normal saline; group II received Azil (10\u00a0mg\/kg, p.o.); group III received 3-NP (10\u00a0mg\/kg, i.p); group IV and V received Azil (5 or 10\u00a0mg\/kg, p.o, respectively) 1\u00a0h prior to 3-NP injection. Both doses of Azil markedly attenuated motor and behavioural dysfunction as well as striatal histopathological alterations caused by 3-NP. In addition, Azil balanced striatal neurotransmitters levels as evidenced by the increase of striatal gamma-aminobutyric acid content and the decrease of glutamate content. Azil also amended neuroinflammation and oxidative stress via modulating I\u0138B\/NF-\u0138B and KEAP1\/Nrf2 downstream signalling pathways, as well as reducing iNOS and COX2 levels. Moreover, Azil demonstrated an anti-apoptotic activity by reducing caspase-3 level and BAX\/BCL2 ratio. In conclusion, the present study reveals the neuroprotective potential of Azil in 3-NP-induced behavioural, histopathological and biochemical changes in rats. These findings might be attributed to inhibition of ATR1\/NF-\u03baB signalling, modulation of Nrf2\/KEAP1 signalling, anti-inflammatory, anti-oxidant and anti-apoptotic properties.<\/jats:p>\n                <jats:p><jats:bold>Graphical Abstract<\/jats:bold><\/jats:p>","DOI":"10.1007\/s11064-023-04083-8","type":"journal-article","created":{"date-parts":[[2024,1,7]],"date-time":"2024-01-07T10:01:45Z","timestamp":1704621705000},"page":"1017-1033","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Azilsartan Attenuates 3-Nitropropinoic Acid-Induced Neurotoxicity in Rats: The Role of I\u0138B\/NF-\u0138B and KEAP1\/Nrf2 Signaling Pathways"],"prefix":"10.1007","volume":"49","author":[{"given":"Hend A.","family":"Hamouda","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rabab H.","family":"Sayed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nihad I.","family":"Eid","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bahia M.","family":"El-Sayeh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,1,7]]},"reference":[{"key":"4083_CR1","doi-asserted-by":"publisher","first-page":"971","DOI":"10.1016\/0092-8674(93)90585-E","volume":"72","author":"ME MacDonald","year":"1993","unstructured":"MacDonald ME, Ambrose CM, Duyao MP, Myers RH, Lin C, Srinidhi L et al (1993) A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington\u2019s disease chromosomes. 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