Timeline showing a summary of the experimental design.

<p>G: gestational age; P: postnatal age (days). PS: prenatal restraint stress; OFT: open field test.</p

Effects of prenatal stress on the body weights of offspring.

<p>A: Weekly body weights of female offspring from PND 0 to PND 28. B: Weekly body weights of male offspring from PND 0 to PND 28. C: Body weights of both sexes on PND 28. Values represent means ± SEM. n=10 per group. <b>^<i>#</i></b><i>p</i><0.05 vs female.</p

Effects of prenatal stress on the open field test.

<p>A: The number of grid crossings of both sexes. B: The rearing counts of both sexes. Values represent means ± SEM. n=10 per group. <b>^<i>*</i></b><i>p</i><0.05 vs CON, ^**<i>p</i><0.01 vs CON, ⁺<i>p</i><0.05 vs CON, ⁺⁺<i>p</i><0.01 vs PS+NS.</p

Effects of prenatal stress on the sucrose preference test.

<p>A: The percentage of sucrose consumed of female offspring at sucrose concentrations of 1 - 32%. B: The percentage of sucrose consumed of male offspring at sucrose concentrations of 1 - 32%. C: The percentage of sucrose consumed of both sexes at sucrose concentrations of 1%. D: The percentage of sucrose consumed of both sexes at sucrose concentrations of 32%. Values represent means ± SEM. n=10 per group. <b>^<i>*</i></b><i>p</i><0.05 vs CON, ⁺<i>p</i><0.05 vs PS+NS.</p

Effects of prenatal stress on the expression of NR2A.

<p>A: NR2A levels in the hippocampus. B: NR2A levels in the frontal cortex. C: NR2A levels in the striatum. Values represent means ± SEM. n=10 per group. ^**p<0.01 vs CON, ⁺⁺<i>p</i><0.01 vs PS+NS.</p

Effects of prenatal stress on the expression of NR1.

<p>A: NR1 levels in the hippocampus. B: NR1 levels in the frontal cortex. C: NR1 levels in the striatum. Values represent means ± SEM. n=10 per group. <b>^<i>*</i></b><i>p</i><0.05 vs CON, ^**<i>p</i><0.01 vs CON, ⁺<i>p</i><0.05 vs CON, ⁺⁺<i>p</i><0.01 vs PS+NS.</p

LC treatment selectively induces expression of p21^cip1 gene, mRNA and protein in cancer cells.

<p>(<b>a</b>) LC induces p21^cip1 gene expression but not p27 and GAPDH. HepG2 cells were treated with LC (2.5, 5.0, 10 mM) for 24 h; cells were collected for gene expression profile analysis. In the gene chip, there are 2 probes for p21^cip1 and 1 probe for p27^kip1. All the fold increases of p21^cip1 and p27^kip1 gene expression <i>versus</i> control were shown. (<b>b</b>) LC dose-dependently induces p21^cip1 mRNA expression but not p27^kip1 in HepG2 cells. HepG2 cells were incubated with different concentrations of LC (2.5, 5, 10 mM) for either 12 h or 24 h; the cells were collected for mRNA assay of p21^cip1 and p27^kip1 by real-time PCR. Fold increase of the LC-treated <i>versus</i> control was shown. Mean+SD (n = 3). *<i>P</i><0.01, **<i>P</i><0.05, compared with control. (<b>c</b>) LC dose-dependently and time-dependently induces p21^cip1 protein accumulation in HepG2 cancer cells. HepG2 and SMMC7721 cells were treated with various doses of LC for 48 h or HepG2 cells were exposed to 5 mM of LC for 12, 24, 36, 48 h; p21 and p27 proteins were detected by Western blot. (<b>d</b>) LC dose-dependently decreases Rb phosphorylation. HepG2 cells were treated with LC for 48 h; Rb and phosphorylated Rb were dectected by Western blot. Typical Western images were shown (left) and band intensity was quantified (right).</p

L-carnitine treatment fails to increase ATP concentration in cancer cells.

<p>(<b>a</b>) Cancer cells are resistant to oligomycin in the presence of D-glucose (2 g/L) but not L-glucose (2 g/L). Human HepG2 cancer cells were cultured in the presence or absence of either D-glucose or L-glucose in the culture medium and treated with various doses of oligomycin (0.1, 0.25, 0.5. 1.0 µg/ml) for 6 h and ATP content was assessed. Mean+SD (n = 3). *<i>P</i><0.01, <i>versus</i> control. DM: DMSO. (<b>b</b>) LC does not increase intracellular ATP content in cancer cells. Human hepatic HepG2 and SMMC-7721 cells were cultured in the normal culture medium respectively and treated with different doses of LC for 6 h, ATP content was detected. LC: L-carnitine. (<b>c</b>) Thymotytes are sensitive to oligomycin in the presence of D-glucose (2 g/L). Mouse thymocytes were treated with oligomycin (1 mg/ml) for different time points (1, 3, 6, 9 h), total ATP content was detected. (<b>d</b>) LC efficiently increases cellular ATP content. Mouse thymocytes were treated with LC (1 mM) for various times, cellular ATP content was assassed. Veh: vehicle.</p

Computional molecular docking of LC with HDAC.

<p>(<b>a</b>) The chemical structure of LC was shown. (<b>b</b>) The docking model of L-carnitine in active site of HDAC.</p

LC induces Histone acetylation in cultured cells.

<p>(<b>a</b>) LC dose-dependently induces accumulation of acetylated histones. HepG2 cells were exposed to LC (1.25, 2.5, 5.0 mM) for 48 h, acetylated histones H3 and H4 were detected by Western blot. GAPDH was used as a loading control. (<b>b</b>) LC time-dependently induces accumulation of acetylated histones. HepG2 cells were treated with LC (5 mM) for different time points (12 h, 24 h, 36 h, 48 h) and acetylated histones were detected. (<b>c</b>) LC treatment increases lysine-acetylated protein accumulation in human HepG2 and SMMC-7721 cancer cells. Human HepG2 and SMMC-7721 cells were treated with LC (10 mM) for 12 h, and then cells were collected for Western blot to detect acetylated proteins with lysine acetylated antibody. (<b>d</b>) LC dose-depentently increases accumulation of acetylated histones in mouse thymocytes. Mouse thymocytes were treated with LC for 24 h, histone acetylation was detected by Western Blot. Buty (1 mM) was used as a positive control.</p