Abstract
We examined the effects of the antioxidant propolis on seizures induced by kainic acid (KA). Sprague-Dawley rats received propolis (75 and 150 mg/kg, p.o.) five times at 12 h intervals. KA (10 mg/kg, i.p.) was injected 1 h after the last propolis treatment. Pretreatment with propolis significantly attenuated KA-induced seizures and KA-induced increases in hippocampal AP-1 DNA binding activity in a dose-dependent manner. KA induced increases in the levels of malondialdehyde and protein carbonyl, and a decrease in the ratio of GSH/GSSG. These oxidative stresses and neuronal degenerations were significantly attenuated by pretreatment with propolis. The neuroprotective effects of propolis appeared to be counteracted by adenosine receptor antagonists [A 1 antagonist, 8-cyclopentyl-1,3-dimethylxanthine (25 or 50 μg/kg) ; A2A antagonist, 1,3,7-trimethyl-8-(3-chlorostyryl)xanthine (0.5 or 1 mg/kg); and A2B antagonist, alloxazine (1.5 or 3.0 mg/kg)]. However, this counteraction was most pronounced in the presence of the A 1 antagonist. Our results suggest that the protective effect of propolis against KA-induced neurotoxic oxidative damage is, at least in part, via adenosine A1 receptor modulation.
| Original language | English |
|---|---|
| Pages (from-to) | 231-235 |
| Number of pages | 5 |
| Journal | Neuroscience Letters |
| Volume | 355 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2004 Jan 30 |
| Externally published | Yes |
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Keywords
- Adenosine receptors
- AP-1 DNA binding activity
- Hippocampus
- Kainate
- Oxidative stress
- Propolis
- Ratio of GSH/GSSG
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Antioxidant propolis attenuates kainate-induced neurotoxicity via adenosine A1 receptor modulation in the rat. / Kwon, Yong Soo; Park, Dae Hun; Shin, Eun Joo; Kwon, Myung Sang; Ko, Kwang Ho; Kim, Won-Ki; Jhoo, Jin Hyeong; Jhoo, Wang Kee; Wie, Myung Bok; Jung, Bae Dong; Kim, Hyoung Chun.
In: Neuroscience Letters, Vol. 355, No. 3, 30.01.2004, p. 231-235.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Antioxidant propolis attenuates kainate-induced neurotoxicity via adenosine A1 receptor modulation in the rat
AU - Kwon, Yong Soo
AU - Park, Dae Hun
AU - Shin, Eun Joo
AU - Kwon, Myung Sang
AU - Ko, Kwang Ho
AU - Kim, Won-Ki
AU - Jhoo, Jin Hyeong
AU - Jhoo, Wang Kee
AU - Wie, Myung Bok
AU - Jung, Bae Dong
AU - Kim, Hyoung Chun
PY - 2004/1/30
Y1 - 2004/1/30
N2 - We examined the effects of the antioxidant propolis on seizures induced by kainic acid (KA). Sprague-Dawley rats received propolis (75 and 150 mg/kg, p.o.) five times at 12 h intervals. KA (10 mg/kg, i.p.) was injected 1 h after the last propolis treatment. Pretreatment with propolis significantly attenuated KA-induced seizures and KA-induced increases in hippocampal AP-1 DNA binding activity in a dose-dependent manner. KA induced increases in the levels of malondialdehyde and protein carbonyl, and a decrease in the ratio of GSH/GSSG. These oxidative stresses and neuronal degenerations were significantly attenuated by pretreatment with propolis. The neuroprotective effects of propolis appeared to be counteracted by adenosine receptor antagonists [A 1 antagonist, 8-cyclopentyl-1,3-dimethylxanthine (25 or 50 μg/kg) ; A2A antagonist, 1,3,7-trimethyl-8-(3-chlorostyryl)xanthine (0.5 or 1 mg/kg); and A2B antagonist, alloxazine (1.5 or 3.0 mg/kg)]. However, this counteraction was most pronounced in the presence of the A 1 antagonist. Our results suggest that the protective effect of propolis against KA-induced neurotoxic oxidative damage is, at least in part, via adenosine A1 receptor modulation.
AB - We examined the effects of the antioxidant propolis on seizures induced by kainic acid (KA). Sprague-Dawley rats received propolis (75 and 150 mg/kg, p.o.) five times at 12 h intervals. KA (10 mg/kg, i.p.) was injected 1 h after the last propolis treatment. Pretreatment with propolis significantly attenuated KA-induced seizures and KA-induced increases in hippocampal AP-1 DNA binding activity in a dose-dependent manner. KA induced increases in the levels of malondialdehyde and protein carbonyl, and a decrease in the ratio of GSH/GSSG. These oxidative stresses and neuronal degenerations were significantly attenuated by pretreatment with propolis. The neuroprotective effects of propolis appeared to be counteracted by adenosine receptor antagonists [A 1 antagonist, 8-cyclopentyl-1,3-dimethylxanthine (25 or 50 μg/kg) ; A2A antagonist, 1,3,7-trimethyl-8-(3-chlorostyryl)xanthine (0.5 or 1 mg/kg); and A2B antagonist, alloxazine (1.5 or 3.0 mg/kg)]. However, this counteraction was most pronounced in the presence of the A 1 antagonist. Our results suggest that the protective effect of propolis against KA-induced neurotoxic oxidative damage is, at least in part, via adenosine A1 receptor modulation.
KW - Adenosine receptors
KW - AP-1 DNA binding activity
KW - Hippocampus
KW - Kainate
KW - Oxidative stress
KW - Propolis
KW - Ratio of GSH/GSSG
UR - http://www.scopus.com/inward/record.url?scp=12144288041&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=12144288041&partnerID=8YFLogxK
U2 - 10.1016/j.neulet.2003.10.075
DO - 10.1016/j.neulet.2003.10.075
M3 - Article
C2 - 14732473
AN - SCOPUS:12144288041
VL - 355
SP - 231
EP - 235
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 3
ER -