ABSTRACT
OBJECTIVE@#To investigate the effect and underlying mechanisms of Tiaoxin Recipe (a Chinese herbal formula) treatment on Alzheimer's disease (AD).@*METHODS@#Twelve-week-old APPswe/PS1ΔE9 (APP/PS1) double transgenic mice were used as a model of AD-afflicted mice. One group of mice was treated with Tiaoxin Recipe by gastrogavage for 12 weeks, while two other groups were given intraperitoneal injections of nicotinamide adenine dinucleotide or FK866 for 4 weeks. Morris water maze and thioflavin S staining tests were performed to evaluate cognitive impairment and amyloid plaque deposition, respectively. Serum amyloid-β1-42 (Aβ1-42) content was detected using an enzyme-linked immunosorbent assay, and quantitative reverse transcription-polymerase chain reaction was performed to examine the expression levels of microRNA-34a (miR-34a) in cortex and hippocampus samples of the study mice.@*RESULTS@#Compared with the normal control group, the memory and learning abilities of the APP/PS1 model group were found to be impaired (P < 0.01), as shown by the increased levels of senile plaque deposition in cortex and hippocampus (P < 0.01), miR-34a expression (P < 0.01) and serum Aβ1-42 content (P < 0.01). Treatment with Tiaoxin Recipe significantly reduced memory impairment (P < 0.01) by reducing amyloid plaque accumulation in cortex and hippocampus (P < 0.01), miR-34a expression (P < 0.01) and serum Aβ1-42 content (P < 0.01) in APP/PS1 mice.@*CONCLUSION@#Tiaoxin Recipe is a viable complementary or alternative therapeutic treatment that is capable of delaying the development of early-stage AD by inhibiting the expression of miR-34a.
ABSTRACT
Objective To investigate the effect of active fraction A (TXR-A) extracted from Tiaoxin Recipe (TXR) on inhibition of corticosterone on long-term potentiation (LTP) induced by high frequency stimulation (HFS) in rat hippocampal slices. Methods The slices were divided into control, corticosterone, corticosterone+TXR, and corticosterone+different concentration of TXR-A groups, then were incubated with artificial cerebrospinal fluid (ACSF) added by drugs for 1 h before recording and were perfused with the same ACSF during recording. Population spike (PS) was recorded from stratum pyramidale of area CA1 using extracellular recording following stimulation of Schaffer collaterals in rat hippocampal slices. Then a 100 Hz, 100 pulses HFS was used to induce LTP. Results PS amplitude was decreased significantly vs that in the control group, when the slices were pre-incubated in ACSF added by corticosterone (2 ?mol/L) over 1.5 h, meaning that LTP was inhibited by corticosterone. However, PS amplitude of the slices pre-incubated in ACSF added by corticosterone (2 ?mol/L) and high concentration TXR-A was increased significantly vs that of corticosterone pre-treating slices, meaning that high concentration TXR-A enhanced LTP inhibited by corticosterone. Furthermore, increased LTP amplitude in high concentration TXR-A was much more than that in TXR. Conclusion TXR-A is one of main TXR active ingredients which facilitate LTP inhibited by corticosterone in area CA1 of rat hippocampal slices. The antagonist (effect) on corticosterone inhibition on LTP is one of the mechanisms to benefit the intelligence.