Novel derivative of Paeonol, Paeononlsilatie sodium, alleviates behavioral damage and hippocampal dendritic injury in Alzheimer's disease concurrent with cofilin1/phosphorylated-cofilin1 and RAC1/CDC42 alterations in rats - Fig 1

<p><b>Effects of Pa on the behavioral performances in the OFT (A-C), EPMT (D-F) and MWMT (G, H)</b> (n = 8–10). Pa treatment (50 mg/kg, i.p.) attenuated the <i>D</i>-gal and AlCl₃-induced decrease in the number of squares crossed (<b>A</b>), the number of clean movements (<b>B</b>), and the number of rears (<b>C</b>) in the OFT. In the EPMT, <i>D</i>-gal and AlCl₃ induced a decrease in the time spent in open arms (<b>D</b>), which was not significantly improved by Pa treatment. However, Pa attenuated the decrease in the number of head dipping (<b>F</b>) and alleviated the increase in the time spent in closed arms (<b>E</b>). (<b>G</b>) The average escape latencies of four acquisition trials per day in DA rats from days 3 to 5 were significantly more than those in CG rats. Pa pretreatment for 6 weeks produced significant protective effects, particularly at days 4~5. (<b>H</b>) Probe trials 24 h after acquisition trials indicated that animals in Pa6 pre-treated with Pa for 6 weeks spent more time in the target quadrant than animals in DA. Data expressed as the means ± SEM. *<i>P<</i>0.05, **<i>P<</i>0.01, ***<i>P<</i>0.001, DA versus CG; ^#<i>P<</i>0.05, ^##<i>P<</i>0.01, ^###<i>P<</i>0.001, Pa2 versus CG; ^ΦΦΦ<i>P<</i>0.001, Pa6 versus CG; ^Δ<i>P<</i>0.05, ^ΔΔΔ<i>P<</i>0.001, DA versus Pa2; ^$<i>P<</i>0.05, ^$$<i>P<</i>0.01, ^$$$<i>P<</i>0.01, DA versus Pa6; ^&&<i>P<</i>0.01, ^&&&<i>P<</i>0.001, Pa2 versus Pa6.