Acidosis induces autophagic cell death through ASIC1-mediated Akt/mTOR signaling in HT22 neurons.

Although it has been confirmed that acid-sensing ion channel 1 (ASIC1) plays a critical role in acidosis-induced neuronal injury and death, its underlying mechanisms remain largely unclear. In the present study, we investigated the involvement of ASIC1 in acidosis-induced neuronal death and its underlying mechanisms in HT22 neurons. The neurons were cultured in acidic medium to mimic extracellular acidosis.

Artemisinin ameliorates cognitive decline by inhibiting hippocampal neuronal ferroptosis via Nrf2 activation in T2DM mice.

Background: Neuronal ferroptosis plays a critical role in the pathogenesis of cognitive deficits. The present study explored whether artemisinin protected type 2 diabetes mellitus (T2DM) mice from cognitive impairments by attenuating neuronal ferroptosis in the hippocampal CA1 region.

Methods: STZ-induced T2DM mice were treated with artemisinin (40 mg/kg, i.

Corticosterone induces neurotoxicity in PC12 cells via disrupting autophagy flux mediated by AMPK/mTOR signaling.

Aims: Our previous study indicated that chronic stress caused autophagy impairment and subsequent neuron apoptosis in hippocampus. However, the mechanism underlying the stress-induced damage to neurons is unclear. In present work, we investigated whether stress-level glucocorticoids (GCs) GCs promoted PC12 cell damage via AMPK/mTOR signaling-mediated autophagy.

Oxidized low-density lipoprotein induced mouse hippocampal HT-22 cell damage via promoting the shift from autophagy to apoptosis.

Aims: Although oxidized low-density lipoprotein (ox-LDL) in the brain induces neuronal death, the mechanism underlying the damage effects remains largely unknown. Given that the ultimate outcome of a cell is depended on the balance between autophagy and apoptosis, this study was performed to explore whether ox-LDL induced HT-22 neuronal cell damage via autophagy impairment and apoptosis enhancement.

Methods: Flow cytometry and transmission electron microscopy (TEM) were used to evaluate changes in cell apoptosis and autophagy, respectively.

Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux.

Epigallocatechin gallate (EGCG) is a major polyphenol in green tea with beneficial effects on the impairment in learning and memory. Autophagy is a cellular process that protects neurons from stressful conditions. The present study was designed to investigate whether EGCG can rescue chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and whether its protective effect involves improvement of autophagic flux.

[Effect of panax notoginseng saponins injection on brain edema in intracerebral hemorrhage rats].

Objective: To study the effect of panax notoginseng saponins (PNS) in treating hemorrhagic apoplexy at super-early stage in rats.

Methods: Rat model of hypertension with cerebral hemorrhage was induced by collagenase method. Sixty rats were randomly divided into 5 groups: the sham operated group, model group, PNS high, middle, and low dose group, 12 in each; 4 h after modeling, PNS or normal saline was intraperitoneally injected into the rats every 12 h, the total is 5 times.