Chinese herbal compound Jinsiwei improves synaptic plasticity in mice with sporadic Alzheimer's disease induced by streptozotocin

Jinsiwei can alleviate learning and memory impairments in a mouse model of SAD, increase the number of synapses and enhance synaptic plasticity rescuing the expression of drebrin, syn, and NR2B and inhibiting cofilin expression.

Seventy-five C57/BL6J male mice were intracerebroventricularly injected with streptozotocin to establish the animal model of SAD. Mice were randomly divided into the model group (MG), donepezil group (DG), and the Jinsiwei high, medium, and low-dose groups (JH, JM, JL). Another fifteen C57/BL6J male mice were injected with artificial cerebrospinal fluid as the control group (CG). The intervention groups were intragastrically administrated with corresponding medicine, while the CG and MG were given 0.5% carboxymethyl cellulose by gavage. After 3 months, the Morris Water Maze test and step-down passive avoidance test were used to assess the learning and memory ability of mice. Synapses in hippocampal CA1 were observed by transmission electron microscope. Immunohistochemistry and western blotting were used to assess the distribution and expression levels of synaptic plasticity-related structural and functional proteins involving drebrin, cofilin, synapsin (syn), and N-methyl D-aspartate receptor subtype 2B (NR2B).

To investigate the efficacy of Jinsiwei (a patented Chinese herbal compound) on learning and memory impairment, the number of synapses and synaptic plasticity-related structural and functional protein expression in mice with sporadic Alzheimer's disease (SAD) induced by streptozotocin.

The Morris Water Maze results showed that the escape latency in the Jinsiwei intervention groups was significantly shorter than that of the MG. Results of the step-down passive-avoidance test showed that the error times in the Jinsiwei intervention groups were significantly reduced compared with the MG. Transmission electron microscope results showed that the number of synapses in hippocampal CA1 was obviously increased in the Jinsiwei intervention groups compared with the MG. Immunohistochemical and western blotting results revealed that the positive cells and expression levels of drebrin, syn, and NR2B were significantly decreased in the MG and meanwhile cofilin significantly increased, while these changes were reversed after the Jinsiwei treatment. Conclusions: Jinsiwei can alleviate learning and memory impairments in a mouse model of SAD, increase the number of synapses and enhance synaptic plasticity rescuing the expression of drebrin, syn, and NR2B and inhibiting cofilin expression.