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Paeoniflorin, the main active component of the peony plant, exerts various pharmacological effects. Recently, research on the effect of paeoniflorin on the nervous system has gained more attention. The aim of the present study was to determine whether paeoniflorin exerts a protective effect that improves Alzheimer's disease (AD) via inflammation and apoptosis in the cerebral cortex of a transgenic mouse model of AD. Transgenic mice were used to construct the model of AD and were treated with paeoniflorin. The Morris water maze test was used to analyze cognitive function in AD mice. The protein expression levels of nuclear factor‑κB, tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and caspase‑3 were examined with commercial kits. Expression levels of B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein (Bax), phosphorylated (p)‑Akt and p‑p38 mitogen‑activated protein kinase (p‑p38 MAPK) in AD were evaluated by western blotting. The neuroprotective effects of paeoniflorin significantly improved cognitive function and ameliorated patterns of escape distance and escape latency in AD mice. Furthermore, the effects of paeoniflorin decreased inflammation and caspase‑3 activity, and inhibited cell death via increasing the Bcl‑2/Bax ratio and p‑Akt expression levels, and downregulating p‑p38 MAPK expression in AD mice.

Resveratrol has also been approved for use in enhancing plant disease resistance and reducing pesticide use. A number of studies have shown that the disease resistance of crops treated with resveratrol is markedly improved. The aim of the present study was to examine the protective effect of resveratrol against alcohol‑induced neurodegeneration occurred and its association with AMP‑activated protein kinase (AMPK)/sirtuin 1 (SIRT1)/p38 in rats and humans. ELISA, caspase‑3 activity and western blot analyses were employed in the present study. Sprague‑Dawley rats and human neuroblastoma SH‑SY5Y cells were treated with alcohol to establish the alcohol‑induced model. Resveratrol protected against alcohol‑induced neuron damage in the hippocampus of the rats. Treatment with resveratrol also inhibited the alcohol‑induced inflammatory response, oxidative stress, caspase‑3 activities and B‑cell lymphoma (Bcl‑2)‑associated X protein/Bcl‑2 in the alcohol‑induced rat. Resveratrol also reduced the upregulated protein expression of AMPK and SIRT1, preventing the pro‑apoptotic alcohol‑induced protein expression of p38 in the rats exposed to alcohol. The downregulation of AMPK suppressed the expression of SIRT1 and activated the expression of p38 in the SH‑SY5Y cell model. Taken together, the data obtained suggested that resveratrol protected against alcohol‑induced neurodegeneration via the AMPK/SIRT1/p38 pathway in rats and humans.

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