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 amyloid‑β (Aβ) and neuroinflammation are two major events in AD. Aβ‑induced 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. Aβ40 and Aβ42 protein levels were detected using western blotting. Production of pro‑inflammatory factors [tumor necrosis factor (TNF)‑α and interleukin (IL)‑1β] 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‑(4,5‑dimethyl‑2‑thiazolyl)‑2,5‑​diphenyl‑2‑H‑tetrazolium bromide assay and flow cytometry analysis respectively. Results demonstrated that CPCGI administration reduced Aβ40 and Aβ42 accumulation, and inhibited inflammatory response and oxidative stress in the in vivo rat model of AD, evidenced by decreased Aβ40 and Aβ42 protein expression, reduced levels of TNF‑α and IL‑1β, reduced MDA content, enhanced SOD activity, and reduced ROS level. It was found that CPCGI enhanced cell viability and reduced cell apoptosis of Aβ25‑35 induced PC12 cells. In addition, the mitogen‑activated protein kinase/NF‑κB 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 Aβ accumulation, inhibiting inflammatory response and oxidative stress, In addition to preventing neuronal apoptosis.