Isorhamnetin ameliorates dopaminergic neuronal damage via targeting FOSL1 to activate AKT/mTOR in 6-OHDA-induced SH-SY5Y cells.

Parkinson's disease (PD) is a chronic neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra compacta, which may result from mitochondrial dysfunction and oxidative stress. Isorhamnetin (Iso) has important antioxidative stress and antiapoptotic effects, this study investigated the effects of Iso on PD in vitro and its underlying mechanisms using a model of 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y cell damage. The results showed that Iso significantly ameliorated 6-OHDA-induced SH-SY5Y cell injury, including decreased cell viability, increased apoptosis and senescence, and oxidative stress injury.

Wuzi Yanzong Pill relieves MPTP-induced motor dysfunction and neuron loss by inhibiting NLRP3 inflammasome-mediated neuroinflammation.

Parkinson disease (PD) is an age-related neurodegenerative disease, which is associated with the loss of dopaminergic neurons (DA neurons) in the substantia nigra pars compacta (SNpc), and neuroinflammation may lead to the occurrence of PD. Wuzi Yanzong Pill (WYP) has demonstrated neuroprotective and anti-inflammatory properties, but its molecular mechanism of action is still unclear. In this study, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice and LPS-mediated BV2 microglia to explore WYP intervention, anti-inflammatory effect and molecular mechanism in vivo and in vitro.

Protocatechuic acid attenuates β‑secretase activity and okadaic acid‑induced autophagy via the Akt/GSK‑3β/MEF2D pathway in PC12 cells.

Okadaic acid (OA) can be used to induce an Alzheimer's disease (AD) model characterized by tau hyperphosphorylation, the formation of neurofibrillary tangles formation and β‑amyloid (Aβ) deposition. Previous studies have shown that the upregulation of Beclin‑1‑dependent autophagy may contribute to the elimination of aggregated Aβ. However, the effects of protocatechuic acid (PA) on the levels of Aβ42, phosphorylated (p)‑tau and β‑secretase in OA‑induced cell injury are unclear, and little is known concerning the role of the PA signaling pathway in the regulation of autophagy.