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Neuroprotective effects of α-tocotrienol on kainic acid-induced neurotoxicity in organotypic hippocampal slice cultures.

Jung NY, Lee KH, Won R, Lee BH - Int J Mol Sci (2013)

Bottom Line: Both co-treatment and post-treatment of ATPH (100 µM) or ATTN (100 µM) significantly increased the cell survival and reduced the number of TUNEL-positive cells in the CA3 region.These data suggest that ATPH and ATTN treatment have protective effects on KA-induced cell death in OHSC.ATTN treatment tended to be more effective than ATPH treatment, even though there was no significant difference between ATPH and ATTN in co-treatment or post-treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, Korea. bhlee@yuhs.ac.

ABSTRACT
Vitamin E, such as alpha-tocopherol (ATPH) and alpha-tocotrienol (ATTN), is a chain-breaking antioxidant that prevents the chain propagation step during lipid peroxidation. In the present study, we investigated the effects of ATTN on KA-induced neuronal death using organotypic hippocampal slice culture (OHSC) and compared the neuroprotective effects of ATTN and ATPH. After 15 h KA (5 µM) treatment, delayed neuronal death was detected in the CA3 region and reactive oxygen species (ROS) formation and lipid peroxidation were also increased. Both co-treatment and post-treatment of ATPH (100 µM) or ATTN (100 µM) significantly increased the cell survival and reduced the number of TUNEL-positive cells in the CA3 region. Increased dichlorofluorescein (DCF) fluorescence and levels of thiobarbiturate reactive substances (TBARS) were decreased by ATPH and ATTN treatment. These data suggest that ATPH and ATTN treatment have protective effects on KA-induced cell death in OHSC. ATTN treatment tended to be more effective than ATPH treatment, even though there was no significant difference between ATPH and ATTN in co-treatment or post-treatment.

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Effects of ATPH (A) and ATTN (B) on KA-induced increase in lipid peroxidation in OHSC. Lipid peroxidation was measured at 24 h recovery time after drugs treatment by TBARS assay as described in Methods. Results are expressed as percentage of control values and are means ± S.E.M. of 9 to 12 experiments. Asterisks (*) indicate statistically significant difference from control (* p < 0.05); Sharps (#) indicate statistically significant difference from KA-treated cultures (#p < 0.05).
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f4-ijms-14-18256: Effects of ATPH (A) and ATTN (B) on KA-induced increase in lipid peroxidation in OHSC. Lipid peroxidation was measured at 24 h recovery time after drugs treatment by TBARS assay as described in Methods. Results are expressed as percentage of control values and are means ± S.E.M. of 9 to 12 experiments. Asterisks (*) indicate statistically significant difference from control (* p < 0.05); Sharps (#) indicate statistically significant difference from KA-treated cultures (#p < 0.05).

Mentions: The extent of lipid peroxidation was determined by the concentration of malondialdehyde (MDA), which is one of the end products of lipid peroxidation measured by the Thiobarbituric acid reactive substances (TBARS) assay. In KA-treated cultures, the levels of MDA were significantly elevated relative to those in the controls (Figure 4). After ATPH or ATTN co-treatment or post-treatment with KA, MDA levels tended to be lower compared to those in cultures treated with KA only. Moreover, in co-treatment or post-treatment of ATPH versus ATTN, although both showed a tendency to reduce MDA levels, ATTN showed statistically significant reduction in the level of MDA.


Neuroprotective effects of α-tocotrienol on kainic acid-induced neurotoxicity in organotypic hippocampal slice cultures.

Jung NY, Lee KH, Won R, Lee BH - Int J Mol Sci (2013)

Effects of ATPH (A) and ATTN (B) on KA-induced increase in lipid peroxidation in OHSC. Lipid peroxidation was measured at 24 h recovery time after drugs treatment by TBARS assay as described in Methods. Results are expressed as percentage of control values and are means ± S.E.M. of 9 to 12 experiments. Asterisks (*) indicate statistically significant difference from control (* p < 0.05); Sharps (#) indicate statistically significant difference from KA-treated cultures (#p < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3794779&req=5

f4-ijms-14-18256: Effects of ATPH (A) and ATTN (B) on KA-induced increase in lipid peroxidation in OHSC. Lipid peroxidation was measured at 24 h recovery time after drugs treatment by TBARS assay as described in Methods. Results are expressed as percentage of control values and are means ± S.E.M. of 9 to 12 experiments. Asterisks (*) indicate statistically significant difference from control (* p < 0.05); Sharps (#) indicate statistically significant difference from KA-treated cultures (#p < 0.05).
Mentions: The extent of lipid peroxidation was determined by the concentration of malondialdehyde (MDA), which is one of the end products of lipid peroxidation measured by the Thiobarbituric acid reactive substances (TBARS) assay. In KA-treated cultures, the levels of MDA were significantly elevated relative to those in the controls (Figure 4). After ATPH or ATTN co-treatment or post-treatment with KA, MDA levels tended to be lower compared to those in cultures treated with KA only. Moreover, in co-treatment or post-treatment of ATPH versus ATTN, although both showed a tendency to reduce MDA levels, ATTN showed statistically significant reduction in the level of MDA.

Bottom Line: Both co-treatment and post-treatment of ATPH (100 µM) or ATTN (100 µM) significantly increased the cell survival and reduced the number of TUNEL-positive cells in the CA3 region.These data suggest that ATPH and ATTN treatment have protective effects on KA-induced cell death in OHSC.ATTN treatment tended to be more effective than ATPH treatment, even though there was no significant difference between ATPH and ATTN in co-treatment or post-treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, Korea. bhlee@yuhs.ac.

ABSTRACT
Vitamin E, such as alpha-tocopherol (ATPH) and alpha-tocotrienol (ATTN), is a chain-breaking antioxidant that prevents the chain propagation step during lipid peroxidation. In the present study, we investigated the effects of ATTN on KA-induced neuronal death using organotypic hippocampal slice culture (OHSC) and compared the neuroprotective effects of ATTN and ATPH. After 15 h KA (5 µM) treatment, delayed neuronal death was detected in the CA3 region and reactive oxygen species (ROS) formation and lipid peroxidation were also increased. Both co-treatment and post-treatment of ATPH (100 µM) or ATTN (100 µM) significantly increased the cell survival and reduced the number of TUNEL-positive cells in the CA3 region. Increased dichlorofluorescein (DCF) fluorescence and levels of thiobarbiturate reactive substances (TBARS) were decreased by ATPH and ATTN treatment. These data suggest that ATPH and ATTN treatment have protective effects on KA-induced cell death in OHSC. ATTN treatment tended to be more effective than ATPH treatment, even though there was no significant difference between ATPH and ATTN in co-treatment or post-treatment.

Show MeSH