Alzheimer's disease (AD), a common neurodegenerative disease, is characterised by the deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles. An increasing number of studies have demonstrated that Aβ causes neuronal damage and mitochondrial dysfunction. Herein, we evaluated the neuroprotective effect of sodium butyrate (NaB) against Aβ induced neurotoxicity in PC12 cells. The results revealed that 3 mM of NaB promoted the expression of angiotensin-converting enzyme and brain-derived neurotrophic factor, which exert a neuroprotective effect by activating G protein-coupled receptors. Moreover, NaB could significantly improve mitochondrial dysfunction caused by Aβ. In conclusion, NaB protected PC12 cells from Aβ-induced cell damage, highlighting the potential of NaB in AD treatment.

Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon contaminant that is widely present in environmental sources, including food. This study aims to clarify the effects of B[a]P toxicity on activated mouse T cells in vitro. Our results show that B[a]P markedly inhibited Concanavalin A (ConA)-induced T lymphocyte proliferation and suppressed the production of the cytokines Interferon (IFN)-γ, Interleukin (IL)-2 and IL-4. Western blot and protein-DNA interaction assays were used to study how B[a]P affects signal transduction. The results revealed that B[a]P suppressed the ConA-induced activation of the Ca²⁺/CaM/NFκB and Ca²⁺/CaM/CaN/NFAT signal transduction pathways. These observations indicate that B[a]P has toxic effects on activated mouse T cells in vitro.