This study investigated the protective effect of Kaempferol against CdCl2-induced hippocampal damage and memory deficit in rats and investigated if such effects involve modulating the activity of AMPK/PTEN/Akt/mTOR axis. Adult male rats (n = 12/group) were divided into control or CdCl2-treated rats received the vehicle of Kaempferol for consecutive 6 weeks. Also, hippocampal cells were treated with CdCl2 in the presence or absence of Kaempferol for 24 h with or without 1 h pre-incubation with compound C, an AMPK inhibitor or with bpV a PTEN inhibitor. Kaempferol improved the behavioral of CdCl2-treated rats, preserved hippocampus structure and reduced hippocampal levels of ROS and protein levels of Bax and cleaved caspase-3. In both control and CdCl2-treated rats, Kaempferol significantly increased hippocampal levels of GSH levels and protein levels of Nfr2, Bcl2 and synaptic proteins (SNAP-25, PSD-25, and synapsin). Concomitantly, it increased the activity of PTEN and AMPK and subsequently, decreased the activity of Akt and mTOR. In cultured cells, individual pharmacological inhibition of PTEN by bpv or AMPK of compound C (CC) partially prevented the stimulatory effect of Kaempferol on Akt/mTOR and its inhibitory effect on cell death whereas a combination of both inhibitors completely prevented this. Also, inhibition of PTEN alone completely abolished the inhibitory effect of Kaempferol by synaptic proteins, whereas inhibition of AMPK completely abolished its stimulatory effect of Nfr2. In conclusion, Kaempferol protects against CdCl2-induced memory deficits and hippocampal apoptosis by its antioxidant potential and inhibition of Akt/mTOR axis and requires the activation of PTEN and AMPK.

中文翻译：

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山萘酚通过增加细胞内谷胱甘肽贮藏和激活PTEN / AMPK诱导的对Akt / mTOR信号的抑制作用来防止氯化镉诱导的记忆丧失和海马细胞凋亡。

这项研究调查了山emp酚对CdCl2诱导的大鼠海马损伤和记忆障碍的保护作用，并研究了这种作用是否涉及调节AMPK / PTEN / Akt / mTOR轴的活性。成年雄性大鼠（n = 12 /组）被分为对照组或经CdCl2处理的大鼠连续6周接受山Ka酚的载体。同样，在有或没有山emp酚的情况下，用CdCl2处理海马细胞24小时，无论是否与化合物C，AMPK抑制剂或bpV PTEN抑制剂预温育1小时。山emp酚改善了CdCl2处理的大鼠的行为，保留了海马结构，降低了海马的ROS水平以及Bax和Caspase-3裂解的蛋白水平。在对照组和CdCl2处理的大鼠中，山萘酚显着提高了海马的GSH水平和Nfr2，Bcl2和突触蛋白（SNAP-25，PSD-25和突触蛋白）的蛋白水平。同时，它增加了PTEN和AMPK的活性，随后降低了Akt和mTOR的活性。在培养的细胞中，化合物C（CC）的bpv或AMPK对PTEN的个别药理抑制作用部分地阻止了山fer酚对Akt / mTOR的刺激作用及其对细胞死亡的抑制作用，而两种抑制剂的组合则完全阻止了这种作用。同样，单独抑制PTEN完全消除了山emp酚对突触蛋白的抑制作用，而对AMPK的抑制则完全消除了Nfr2的刺激作用。结论，