Salviae Miltiorrhizae BGE Radix Increases Rat Striatal K+-Stimulated Dopamine Release and Activates the Dopamine Release with Protection Against Hydrogen Peroxide-Induced Injury in Rat Pheochromocytoma PC12 Cells |
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Authors: | Tae-Wook Chung Byung-Soo Koo Kyeong-Oh Kim Hee-Sang Jeong Min-Gon Kim Kang-Hung Chung In-Seon Lee Cheorl-Ho Kim |
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Institution: | (1) Department of Biological Science, Sungkyunkwan University and National Research Laboratory for Glycobiology, 440-746, Jangan-Gu, Suwon City, Kyunggi-Do, Korea;(2) Department of Oriental Medicine, Dongguk University, 780-714 Kyungju, Kyungbuk, Korea;(3) Department of Oriental Medicine, Dongshin University, 520-714 Naju, Jeonnam, Korea;(4) Nanobiotechnology Research Center, Korea Research Institute of Bioscience and Biotechnology, Yusong-Gu, Daejon , 305-600, Korea;(5) Department of Food Science and Technology, Seoul National University of Technology, Nowon-Gu, Seoul, Korea;(6) The Center of Traditional Microorganisms Resources (TMR), Keimyun University, Daegu, Korea;(7) Department of Biological Science, Sungkyunkwan University, Chunchun-Dong 300, Jangan-Gu, Suwon City, Kyunggi-Do, 440-746, Korea |
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Abstract: | The present study investigated the effect of the medicinal plant Salviae miltiorrhizae radix (SMR) on dopaminergic neurotransmission in comparison with amphetamine. The effect of SM (0.1 g/ml) on K+ (20 mM)-stimulated dopamine (DA) release from rat striatal slices was compared with amphetamine (10−4 M). Amphetamine and SMR significantly increased K+-stimulated DA release (P<0.001) from rat striatal slices when compared with K+-stimulated alone. On the other hand, to examine whether in vitro SMR treatment induces DA release in PC12 cells, the role of protein kinases has been investigated in the induction of the
SMR-mediated events by using inhibitors of protein kinase C (PKC), mitogen activated protein kinase (MAP kinase) or protein
kinase A (PKA). PKC inhibitors chelerythrine (50 and 100 nM), Ro31-8220 (100 nM) and the MAP kinase inhibitor, PD98059 (20 μM)
inhibited the ability of SMR to elicit the SMR-stimulated DA release. The direct-acting PKC activator, 12-O-tetradecanoyl phorbol 13-acetate (TPA, 100 nM) mimicked the ability of SMR to elicit DA release. On the contrary, a selective
PKA inhibitor, 50 μM Rp-8-Br-cAMP, blocked the development of SMR-stimulated DA release. The results demonstrated that SMR
may stimulate DA release and that SMR-induced increases in MAP kinase and PKC are important for induction of the enhancement
in transporter-mediated DA release and PKA was also required for the enhancement in SMR-stimulated DA release. SMR treatment
(0.1–10 μg/ml) to the hydrogen peroxide (H2O2)-treated PC12 cells activated the enzyme activities such as catalase, superoxide dismutase and glutathione peroxidase, and
decreased the malondialdehyde level, indicating that SMR has also protective effects against free radical-induced cell toxicity.
Therefore, the mechanism by which SMR induces the enhancement in SMR-stimulated DA release is apparent. It remains to be determined
whether the effect of SMR on DA function is important in its therapeutic use in the treatment of drug addiction. |
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Keywords: | Salviae miltiorrhizae radix dopamine amphetamine PKC MAP kinase PKA free radicals hydrogen peroxide glutathione peroxidase catalase superoxide dismutase PC12 cells malondialdehyde |
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