Activation of α7nAChR by PNU282987 improves cognitive impairment through inhibiting oxidative stress and neuroinflammation in D-galactose induced aging via regulating α7nAChR/Nrf2/HO-1 signaling pathway

• DOI: 10.1016/j.exger.2023.112139
• Publication Date: 2023-03-10T05:16:54Z
• Authors: Yawen Zhang; Rui Ma; Wencheng Wang; Qian Deng; Chi Cao; Chunyang Yu; Shulin Li; Lei Shi; Jianying Tian
• Keywords: Methyllycaconitine

Aging is an important risk factor for neurodegenerative diseases. The activation of α7 nicotinic acetylcholine receptor (α7nAChR) involved in inflammation and cognition, but the specific role it plays aging remains unknown. This study aimed to investigate anti-aging effect α7nAChR on rats BV2 cells induced by D-galactose, as well its potential mechanism. D-galactose increase SA-β-Gal positive cells, expression p16 p21 vivo vitro. selective agonist PNU282987 decreased levels pro-inflammatory factors, MDA, Aβ, enhanced SOD activity anti-inflammatory (IL10) vivo. Arg1, iNOS, IL1β TNFα upregulated α7nAChR, Nrf2 HO-1 results Morris water maze novel object recognition tests showed that improved cognitive impairment rats. Furthermore, inhibitor methyllycaconitine (MLA) were opposite with PNU282987. improves through inhibiting oxidative stress neuroinflammation via regulating α7nAChR/Nrf2/HO-1 signaling pathway. Therefore, targeting may be a viable therapeutic approach anti-inflammaging