ArticleInflammopharmacology2025
Neuroprotective effects of candesartan in 3-nitropropionic acid-induced Huntington's disease: modulation of angiotensin and CREB/BDNF/PGC1-α signaling.
Article in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Renin-Angiotensin System has been implicated in neurodegenerative diseases such as Huntington's (HD). It is made up of two axes: one is the Angiotensin II Type 1 receptor (AT1R) or Angiotensin II Type 2 receptor (AT2R), while the other is angiotensin-(1-7) [Ang-(1-7)], and Mas receptor; the latter has reported developing a neuroprotective effect; oppositely, AT1R activation has been linked to neurodegenerative diseases. This study aims to elucidate the potential neuroprotective effect of Candesartan (Cand) an AT1R blocker in mitigating neuronal degeneration caused by 3-Nitropropionic acid (3NP) induced HD by revealing the prospective role of Ang II/AT2R/Ang-(1-7)/Mas receptor, CREB/BDNF/PGC1-α besides JNK/c-Jun trajectories, as well as the anti-apoptotic survivin. HD was induced by 3NP (10 mg/kg) for 14 days. Rats received Candesartan (2.5 or 5 mg/kg) for 14 days, after which brain and striatum were isolated for the histopathological, immunohistochemical, and biochemical analysis. Cand displayed significant improvement in the rats' behavioral tests, enhancing their memory, motor, and cognitive functions induced by 3NP, which was confirmed by the striatal histopathological and immunohistochemical examination of the GFAP. In addition, Cand activated the Ang II/AT2R/Ang-(1-7)/Mas receptor axis. Moreover, Cand stimulated the production of striatal neurotrophic proteins CREB/BDNF/PGC1-α which in turn decreased the levels of inflammatory mediators NF-κB and IL-1β, accompanied by an increase in the antioxidants NQO1 and HO-1 levels. Similarly, Cand led to the inhibition of the JNK/c-Jun with activation of survivin. In conclusion, Candesartan has mitigated the striatal degeneration and mitochondrial dysfunction induced by 3NP through various mechanistic pathways.
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