Nicotinamide ameliorates amyloid beta-induced oxidative stress-mediated neuroinflammation and neurodegeneration in adult mouse brain was written by Rehman, Inayat Ur;Ahmad, Riaz;Khan, Ibrahim;Lee, Hyeon Jin;Park, Jungsung;Ullah, Rahat;Choi, Myeong Jun;Kang, Hee Young;Kim, Myeong Ok. And the article was included in Biomedicines in 2021.Formula: C20H10Cl2O5 This article mentions the following:
Alzheimer’s disease (AD) is the most predominant age-related neurodegenerative disease, pathol. characterized by the accumulation of aggregates of amyloid beta Aβ1-42 and tau hyperphosphorylation in the brain. It is considered to be the primary cause of cognitive dysfunction. The aggregation of Aβ1-42 leads to neuronal inflammation and apoptosis. Since vitamins are basic dietary nutrients that organisms need for their growth, survival, and other metabolic functions, in this study, the underlying neuroprotective mechanism of nicotinamide (NAM) Vitamin B3 against Aβ1-42 -induced neurotoxicity was investigated in mouse brains. Intracerebroventricular (i.c.v.) Aβ1-42 injection elicited neuronal dysfunctions that led to memory impairment and neurodegeneration in mouse brains. After 24 h after Aβ1-42 injection, the mice were treated with NAM (250 mg/kg i.p.) for 1 wk. For biochem. and Western blot studies, the mice were directly sacrificed, while for confocal and “immunohistochem. staining”, mice were perfused transcardially with 4% paraformaldehyde. Our biochem., immunofluorescence, and immunohistochem. results showed that NAM can ameliorate neuronal inflammation and apoptosis by reducing oxidative stress through lowering malondialdehyde and 2,7-dichlorofluorescein levels in an Aβ1-42-injected mouse brains, where the regulation of p-JNK further regulated inflammatory marker proteins (TNF-α, IL-1β, transcription factor NF-kB) and apoptotic marker proteins (Bax, caspase 3, PARP1). Furthermore, NAM + Aβ treatment for 1 wk increased the amount of survival neurons and reduced neuronal cell death in Nissl staining. We also analyzed memory dysfunction via behavioral studies and the anal. showed that NAM could prevent Aβ1-42 -induced memory deficits. Collectively, the results of this study suggest that NAM may be a potential preventive and therapeutic candidate for Aβ1-42 -induced reactive oxygen species (ROS)-mediated neuroinflammation, neurodegeneration, and neurotoxicity in an adult mouse model. In the experiment, the researchers used many compounds, for example, 2′,7′-Dichloro-3′,6′-dihydroxy-3H-spiro[isobenzofuran-1,9′-xanthen]-3-one (cas: 76-54-0Formula: C20H10Cl2O5).
2′,7′-Dichloro-3′,6′-dihydroxy-3H-spiro[isobenzofuran-1,9′-xanthen]-3-one (cas: 76-54-0) belongs to benzofurans derivatives. Benzofuran is a core structural unit found in many naturally occurring compounds with multidirectional biological activities. Benzofurans are stable towards alkali and readily polymerize on treatment with sulfuric acid, due to which they are useful for the preparation of low cost chemically relatively inert resins.Formula: C20H10Cl2O5
Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem