Neuroprotective effect of apigenin against cerebral ischemia/reperfusion injury.

OBJECTIVE: The therapeutic efficacy of apigenin in PC12 cells and rats remains uncertain. The aim of this study was to investigate the neuroprotective effects of apigenin against cerebral ischemia/reperfusion injury, both in vitro and in vivo. METHODS: We first treated PC12 cells with cobalt chloride (CoCl2) to create a model of oxidative stress injury. Cell viability was then determined using a multifunctional microplate reader. In addition, reactive oxygen species (ROS) levels, apoptosis, and mitochondrial membrane potentials (MMPs) were examined using high-content cytometer analysis. The efficacy of apigenin treatment was also analyzed in a rat middle cerebral artery occlusion (MCAO) model using TTC staining and neurological deficit scores. RESULTS: The half-inhibitory concentration of CoCl2 was 1.2 mM. Pretreatment with 10 µg ⋅ mL-1 apigenin significantly enhanced cell viability, reduced ROS levels, alleviated apoptosis, and improved MMP in PC12 cells with CoCl2-induced injury in vitro. In addition, apigenin treatment in vivo significantly improved neurological deficit scores and reduced infarct areas in MCAO rats. These results suggest that the neuroprotective mechanisms of apigenin may be related to mitochondrial activation. CONCLUSIONS: Apigenin had excellent neuroprotective effects for the treatment of cerebral ischemia/reperfusion injury in vitro and in vivo.

Neuroprotective effect of CPCGI on Alzheimer's disease and its mechanism.

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder causing progressive memory loss and cognitive impairment. The aberrant accumulation of amyloid­ß (Aß) and neuroinflammation are two major events in AD. Aß­induced neurotoxicity and oxidative stress are also involved in the pathogenesis of AD. The purpose of the current study was to investigate the effect of compound porcine cerebroside and ganglioside injection (CPCGI) on the progression of AD, and to explore the molecular mechanism. In vivo and in vitro models of AD were established and treated with CPCGI. Aß40 and Aß42 protein levels were detected using western blotting. Production of pro­inflammatory factors [tumor necrosis factor (TNF)­α and interleukin (IL)­1ß] and oxidative stress markers [malondialdehyde (MDA), superoxide dismutase (SOD)] and reactive oxygen species (ROS) production were determined. Cell viability and apoptosis were detected using 3­(4,5­dimethyl­2­thiazolyl)­2,5­â€‹diphenyl­2­H­tetrazolium bromide assay and flow cytometry analysis respectively. Results demonstrated that CPCGI administration reduced Aß40 and Aß42 accumulation, and inhibited inflammatory response and oxidative stress in the in vivo rat model of AD, evidenced by decreased Aß40 and Aß42 protein expression, reduced levels of TNF­α and IL­1ß, reduced MDA content, enhanced SOD activity, and reduced ROS level. It was found that CPCGI enhanced cell viability and reduced cell apoptosis of Aß25­35 induced PC12 cells. In addition, the mitogen­activated protein kinase/NF­κB pathway was involved in the protective effect of CPCGI on AD. Taken together, the data demonstrated that CPCGI exerted a protective effect on AD by reducing Aß accumulation, inhibiting inflammatory response and oxidative stress, In addition to preventing neuronal apoptosis.