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Proteomic change by Korean Red Ginseng in the substantia nigra of a Parkinson's disease mouse model
Kim, Dongsoo,Kwon, Sunoh,Jeon, Hyongjun,Ryu, Sun,Ha, Ki-Tae,Kim, Seungtae The Korean Society of Ginseng 2018 Journal of Ginseng Research Vol.42 No.4
Background: Recent studies have shown that Korean Red Ginseng (KRG) successfully protects against dopaminergic neuronal death in the nigrostriatal pathway of a Parkinson's disease (PD) mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration; however, the mechanism has yet to be identified. Therefore, in this study we used two-dimensional electrophoresis to investigate the effects of KRG on the changes in protein expression in the substantia nigra (SN) of MPTP-treated mice. Methods: Male C57BL/6 mice (9 wk old) were intraperitoneally administered MPTP (20 mg/kg) four times at 2-h intervals, after which KRG (100 mg/kg) was orally administered once a day for 5 d. Two hours after the fifth KRG administration, a pole test was conducted to evaluate motor function, after which the brains were immediately collected. Survival of dopaminergic neurons was measured by immunohistochemistry, and protein expression was measured by two-dimensional electrophoresis and Western blotting. Results: KRG alleviated MPTP-induced behavioral dysfunction and neuronal toxicity in the SN. Additionally, the expression of eight proteins related to neuronal formation and energy metabolism for survival were shown to have changed significantly in response to MPTP treatment or KRG administration. KRG alleviated the downregulated protein expression following MPTP administration, indicating that it may enhance neuronal development and survival in the SN of MPTP-treated mice. Conclusion: These findings indicate that KRG may have therapeutic potential for the treatment of patients with PD.
Effects of Amyloid-β Peptides on Voltage-Gated L-Type CaV1.2 and CaV1.3 Ca2+ Channels
Sunoh Kim,임혜원 한국분자세포생물학회 2011 Molecules and cells Vol.32 No.3
Overload of intracellular Ca^(2+) has been implicated in the pathogenesis of neuronal disorders, such as Alzheimer’s disease. Various mechanisms produce abnormalities in intracellular Ca^(2+) homeostasis systems. L-type Ca^(2+) channels have been known to be closely involved in the mechanisms underlying the neurodegenerative properties of amyloid-β (Aβ) peptides. However, most studies of L-type Ca^(2+) channels in Aβ-related mechanisms have been limited to Ca_V1.2, and surprisingly little is known about the involvement of Ca_V.1.3 in Aβ-induced neuronal toxicity. In the present study, we examined the expression patterns of CaV1.3 after Aβ_(25-35) exposure for 24 h and compared them with the expression patterns of Ca_V1.2. The expression levels of Ca_V1.3 were not significantly changed by Aβ_(25-35) at both the mRNA levels and the total protein level in cultured hippocampal neurons. However, surface protein levels of Ca_V1.3 were significantly increased by Aβ_(25-35), but not by Aβ_(35-25). We next found that acute treatment with Aβ_(25-35) increased Ca_V1.3 channel activities in HEK293 cells using whole-cell patch-clamp recordings. Furthermore, using GTP pulldown and co-immunoprecipitation assays in HEK293cell lysates, we found that amyloid precursor protein interacts with β_3 subunits of Ca^(2+) channels instead of Ca_V1.2 or Ca_V1.3 α_1 subunits. These results show that Aβ_(25-35) chronically or acutely upregulates Ca_V1.3 in the rat hippocampal and human kidney cells (HEK293). This suggests that Ca_V1.3 has a potential role along with Ca_V1.2 in the pathogenesis of Alzheimer’s disease.