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Royal jelly facilitates restoration of the cognitive ability in trimethyltin-intoxicated mice.

Hattori N, Ohta S, Sakamoto T, Mishima S, Furukawa S - Evid Based Complement Alternat Med (2010)

Bottom Line: Neural stem/progenitor cells (NS/NPCs) are present in the adult hippocampal DG, and generate neurons that can function for the cognition ability.Therefore, we investigated whether royal jelly (RJ) stimulates the regenerating processes of the TMT-injured hippocampal DG, and found that orally administered RJ significantly increased the number of DG granule cells and simultaneously improved the cognitive impairment.Furthermore, we have already shown that RJ facilitates neurogenesis of cultured NS/NPCs.

View Article: PubMed Central - PubMed

Affiliation: Nagaragawa Research Center, API Co., Ltd, Nagara, Gifu 502-0071, Japan.

ABSTRACT
Trimethyltin (TMT) is a toxic organotin compound that induces acute neuronal death selectively in the hippocampal dentate gyrus (DG) followed by cognition impairment; however the TMT-injured hippocampal DG itself is reported to regenerate the neuronal cell layer through rapid enhancement of neurogenesis. Neural stem/progenitor cells (NS/NPCs) are present in the adult hippocampal DG, and generate neurons that can function for the cognition ability. Therefore, we investigated whether royal jelly (RJ) stimulates the regenerating processes of the TMT-injured hippocampal DG, and found that orally administered RJ significantly increased the number of DG granule cells and simultaneously improved the cognitive impairment. Furthermore, we have already shown that RJ facilitates neurogenesis of cultured NS/NPCs. These present results, taken together with previous observations, suggest that the orally administered RJ may be a promising avenue for ameliorating neuronal function by regenerating hippocampal granule cells that function in the cognition process.

No MeSH data available.


Related in: MedlinePlus

Amelioration of the TMT-induced impairment of short-term memory by the feeding with RJ. Mice were processed according to the schedule illustrated in (a). The mice were treated with TMT in PBS or PBS alone on day 0, and feeding with RJ (0, 1 or 5%) for 6 days was started from day 2. The spontaneous alternation behavior test was performed on day 8. The ordinates in (b) and (c) show the total alternation opportunities (total arm entries) and percentage of alternation, respectively, measured for 8 min. The values are expressed as the mean ± SE (n = 8–10). The difference between the control value (PBS-treated mice fed without RJ) and that for the TMT-treated mice fed without RJ diet was significant at *P <  .05 by one-way ANOVA with Holm's test. #P <  .05, TMT-treated mice with versus without RJ (5%).
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fig2: Amelioration of the TMT-induced impairment of short-term memory by the feeding with RJ. Mice were processed according to the schedule illustrated in (a). The mice were treated with TMT in PBS or PBS alone on day 0, and feeding with RJ (0, 1 or 5%) for 6 days was started from day 2. The spontaneous alternation behavior test was performed on day 8. The ordinates in (b) and (c) show the total alternation opportunities (total arm entries) and percentage of alternation, respectively, measured for 8 min. The values are expressed as the mean ± SE (n = 8–10). The difference between the control value (PBS-treated mice fed without RJ) and that for the TMT-treated mice fed without RJ diet was significant at *P <  .05 by one-way ANOVA with Holm's test. #P <  .05, TMT-treated mice with versus without RJ (5%).

Mentions: According to the experimental schedule shown in Figure 2(a), mice were injected with TMT in PBS or PBS alone on day 0 and successively fed the RJ-containing diet for 6 days, from days 2 to 7; and the spontaneous alternation rate and neuronal cell number were then evaluated on day 8. TMT treatment significantly impaired the spontaneous alternation rate when evaluated on day 8; however, the feeding with the diet of 5% RJ, but not 1% RJ, significantly suppressed this impairment (Figure 2(c)). As there was no significant difference in the number of arm entries among the groups (Figure 2(b)), RJ did not affect the locomotion activity. After the behavioral test, the mice were fixed with 4% paraformaldehyde solution, and brain sections were prepared and stained. As shown in Figure 3(A), TMT-treated mice without the RJ diet (A, b) appeared to have a smaller number of neurons than TMT-non-treated mice without the RJ diet (A, a); whereas the TMT-treated mice with the RJ diet (A, c) appeared to have a greater number of neurons than TMT-treated ones without it. Actual cell counting demonstrated that the TMT-induced decrease in the number of neurons on day 8 (Figure 3(B), b) was significantly attenuated by RJ feeding (Figure 3(B), c).


Royal jelly facilitates restoration of the cognitive ability in trimethyltin-intoxicated mice.

Hattori N, Ohta S, Sakamoto T, Mishima S, Furukawa S - Evid Based Complement Alternat Med (2010)

Amelioration of the TMT-induced impairment of short-term memory by the feeding with RJ. Mice were processed according to the schedule illustrated in (a). The mice were treated with TMT in PBS or PBS alone on day 0, and feeding with RJ (0, 1 or 5%) for 6 days was started from day 2. The spontaneous alternation behavior test was performed on day 8. The ordinates in (b) and (c) show the total alternation opportunities (total arm entries) and percentage of alternation, respectively, measured for 8 min. The values are expressed as the mean ± SE (n = 8–10). The difference between the control value (PBS-treated mice fed without RJ) and that for the TMT-treated mice fed without RJ diet was significant at *P <  .05 by one-way ANOVA with Holm's test. #P <  .05, TMT-treated mice with versus without RJ (5%).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3094710&req=5

fig2: Amelioration of the TMT-induced impairment of short-term memory by the feeding with RJ. Mice were processed according to the schedule illustrated in (a). The mice were treated with TMT in PBS or PBS alone on day 0, and feeding with RJ (0, 1 or 5%) for 6 days was started from day 2. The spontaneous alternation behavior test was performed on day 8. The ordinates in (b) and (c) show the total alternation opportunities (total arm entries) and percentage of alternation, respectively, measured for 8 min. The values are expressed as the mean ± SE (n = 8–10). The difference between the control value (PBS-treated mice fed without RJ) and that for the TMT-treated mice fed without RJ diet was significant at *P <  .05 by one-way ANOVA with Holm's test. #P <  .05, TMT-treated mice with versus without RJ (5%).
Mentions: According to the experimental schedule shown in Figure 2(a), mice were injected with TMT in PBS or PBS alone on day 0 and successively fed the RJ-containing diet for 6 days, from days 2 to 7; and the spontaneous alternation rate and neuronal cell number were then evaluated on day 8. TMT treatment significantly impaired the spontaneous alternation rate when evaluated on day 8; however, the feeding with the diet of 5% RJ, but not 1% RJ, significantly suppressed this impairment (Figure 2(c)). As there was no significant difference in the number of arm entries among the groups (Figure 2(b)), RJ did not affect the locomotion activity. After the behavioral test, the mice were fixed with 4% paraformaldehyde solution, and brain sections were prepared and stained. As shown in Figure 3(A), TMT-treated mice without the RJ diet (A, b) appeared to have a smaller number of neurons than TMT-non-treated mice without the RJ diet (A, a); whereas the TMT-treated mice with the RJ diet (A, c) appeared to have a greater number of neurons than TMT-treated ones without it. Actual cell counting demonstrated that the TMT-induced decrease in the number of neurons on day 8 (Figure 3(B), b) was significantly attenuated by RJ feeding (Figure 3(B), c).

Bottom Line: Neural stem/progenitor cells (NS/NPCs) are present in the adult hippocampal DG, and generate neurons that can function for the cognition ability.Therefore, we investigated whether royal jelly (RJ) stimulates the regenerating processes of the TMT-injured hippocampal DG, and found that orally administered RJ significantly increased the number of DG granule cells and simultaneously improved the cognitive impairment.Furthermore, we have already shown that RJ facilitates neurogenesis of cultured NS/NPCs.

View Article: PubMed Central - PubMed

Affiliation: Nagaragawa Research Center, API Co., Ltd, Nagara, Gifu 502-0071, Japan.

ABSTRACT
Trimethyltin (TMT) is a toxic organotin compound that induces acute neuronal death selectively in the hippocampal dentate gyrus (DG) followed by cognition impairment; however the TMT-injured hippocampal DG itself is reported to regenerate the neuronal cell layer through rapid enhancement of neurogenesis. Neural stem/progenitor cells (NS/NPCs) are present in the adult hippocampal DG, and generate neurons that can function for the cognition ability. Therefore, we investigated whether royal jelly (RJ) stimulates the regenerating processes of the TMT-injured hippocampal DG, and found that orally administered RJ significantly increased the number of DG granule cells and simultaneously improved the cognitive impairment. Furthermore, we have already shown that RJ facilitates neurogenesis of cultured NS/NPCs. These present results, taken together with previous observations, suggest that the orally administered RJ may be a promising avenue for ameliorating neuronal function by regenerating hippocampal granule cells that function in the cognition process.

No MeSH data available.


Related in: MedlinePlus