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Cho, Soon Ock,Ban, Ju Yeon,Kim, Joo Youn,Jeong, Ha Yeon,Lee, Ik Soo,Song, Kyung-Sik,Bae, KiHwan,Seong, Yeon Hee The Japanese Pharmacological Society 2009 JOURNAL OF PHARMACOLOGICAL SCIENCES Vol.111 No.1
<P>The present study investigated an ethanol extract of the aerial part of <I>Aralia cordata</I> Thunb. (Araliaceae) for possible neuroprotective effects on neurotoxicity induced by amyloid β (Aβ) protein (25 – 35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to 10 μM Aβ(25 – 35) for 36 h induced neuronal apoptotic death. At 1 – 10 μg/ml, <I>A. cordata</I> inhibited neuronal death, elevation of intracellular calcium ([Ca<SUP>2+</SUP>]<SUB>i</SUB>), glutamate release into the medium, and generation of reactive oxygen species (ROS) induced by Aβ(25–35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol Aβ(25–35) was inhibited by chronic treatment with <I>A. cordata</I> (50 and 100 mg/kg, p.o. for 7 days) as measured by a passive avoidance test, and corresponding reductions were observed in brain cholinesterase activity and neuronal death measured histologically in the hippocampal region. Oleanolic acid isolated from <I>A. cordata</I> also inhibited neuronal death, elevation of [Ca<SUP>2+</SUP>]<SUB>i</SUB>, glutamate release, and generation of ROS induced by Aβ(25–35) in cultured rat cortical neurons, suggesting that the neuroprotective effect of <I>A. cordata</I> may be, at least in part, attributable to this compound. From these results, we suggest that the antidementia effect of <I>A. cordata</I> is due to its neuroprotective effect against Aβ(25–35)-induced neurotoxicity and that <I>A. cordata</I> may have a therapeutic role in preventing the progression of Alzheimer’s disease.</P>
Lee, Chang Ki,Son, Seung Hwa,Park, Kwang Kyun,Park, Jung Han Yoon,Lim, Soon Sung,Chung, Won Yoon The Japanese Pharmacological Society 2008 JOURNAL OF PHARMACOLOGICAL SCIENCES Vol.106 No.3
<P>A growing amount of attention has been focused on the investigation of the effects of chemopreventive agents on the inhibition of cancer cell growth and toxicity in combination with chemotherapeutics. The objective of this study was to determine whether isoliquiritigenin (ISL) has the potential to serve as a beneficial supplement during cisplatin chemotherapy. We found that the administration of ISL alone significantly reduced the size of the solid tumors in CT-26 cell–inoculated BALB/c mice, without any detectable induction of nephrotoxicity, hepatotoxicity, and oxidative stress, and ISL reduced the viability and DNA synthesis of CT-26 murine colon cancer cells in a dose-dependent manner. ISL did not affect the therapeutic efficacy of cisplatin. Furthermore, ISL suppressed cisplatin-induced kidney damage characterized by increases in serum creatinine and blood urea nitrogen, as well as cisplatin-induced liver damage characterized by increases in serum alanine aminotransferase and aspartate aminotransferase. The repeated oral administration of ISL prior to cisplatin treatment exerted a preventive effect on cisplatin-mediated increases in serum nitric oxide and tissue lipid peroxidation levels, and it recovered depleted GSH levels in the tissues. Therefore, supplementation with ISL may be an effective approach to counteracting the side effects of cisplatin therapy in cancer patients.</P>
Shin, Eun-Joo,Jeong, Ji Hoon,Kim, Hyun Ji,Jang, Choon-Gon,Yamada, Kiyofumi,Nabeshima, Toshitaka,Kim, Hyoung-Chun The Japanese Pharmacological Society 2007 Journal of pharmacological sciences Vol.105 No.4
<P>We demonstrated that exposure to extremely low frequency magnetic fields (ELF-MF) enhanced dopamine levels in the rat striatum. To extend our understanding, we examined the role of dopaminergic receptors in ELF-MF–induced behavioral changes. Exposure to ELF-MF (2.4 mT, 1 h/day, for one or seven days) enhanced locomotor activity in a time-dependent manner. This hyperlocomotor activity paralleled an increase in c-Fos-like immunoreactivity (c-Fos-IR). Pretreatment with SCH23390, a dopaminergic D<SUB>1</SUB>-like receptor antagonist, but not with sulpiride, a dopaminergic D<SUB>2</SUB>-like receptor antagonist, inhibited ELF-MF–induced increased locomotor activity and c-Fos-IR. Thus, our results suggest that ELF-MF–induced behavioral responses are, at least in part, mediated by activation of dopamine D<SUB>1</SUB>-like receptors.</P>
Mun, Se Hwan,Kim, Hyuk Soon,Kim, Jie Wan,Ko, Na Young,Kim, Do Kyun,Lee, Beob Yi,Kim, Bokyung,Won, Hyung Sik,Shin, Hwa-Sup,Han, Jeung-Whan,Lee, Hoi Young,Kim, Young Mi,Choi, Wahn Soo The Japanese Pharmacological Society 2009 Journal of pharmacological sciences Vol.111 No.1
<P>We investigated whether oral administration of curcumin suppressed type II collagen–induced arthritis (CIA) in mice and its effect and mechanism on matrix metalloproteinase (MMP)-1 and MMP-3 production in CIA mice, RA fibroblast-like synoviocytes (FLS), and chondrocytes. CIA in mice was suppressed by oral administration of curcumin in a dose-dependent manner. Macroscopic observations were confirmed by histological examinations. Histological changes including infiltration of immune cells, synovial hyperplasia, cartilage destruction, and bone erosion in the hind paw sections were extensively suppressed by curcumin. The histological scores were consistent with clinical arthritis indexes. Production of MMP-1 and MMP-3 were inhibited by curcumin in CIA hind paw sections and tumor necrosis factor (TNF)-α–stimulated FLS and chondrocytes in a dose-dependent manner. As for the mechanism, curcumin inhibited activating phosphorylation of protein kinase Cδ (PKCδ) in CIA, FLS, and chondrocytes. Curcumin also suppressed the JNK and c-Jun activation in those cells. This study suggests that the suppression of MMP-1 and MMP-3 production by curcumin in CIA is mediated through the inhibition of PKCδ and the JNK/c-Jun signaling pathway.</P>
Yeom, Mi-Jung,Lee, Han-Chang,Kim, Gun-Ho,Lee, Hye-Jung,Shim, Insop,Oh, Seung-Kyu,Kang, Sung-Keel,Hahm, Dae-Hyun The Japanese Pharmacological Society 2006 JOURNAL OF PHARMACOLOGICAL SCIENCES Vol.100 No.1
<P>Anti-inflammatory and anti-arthritic effects of water distillates of <I>Ephedra sinica</I> S<SMALL>TAPF</SMALL> (ES), in herb-acupuncture, on the inflammatory responses of arthritis was investigated using phorbol 12-myristate 13-acetate (PMA)/lipopolysaccharide (LPS)-induced human macrophage and adjuvant-induced arthritic rat. The luciferase reporter vectors driven by the tumor necrosis factor (TNF)-α and cyclooxygenase-2 promoters were transiently transfected into U937 cells, which were then differentiated and stimulated by PMA and LPS, respectively, to develop an in vitro anti-inflammation assay system. The luciferase activities, observed in the activated U937 cells, were significantly inhibited by ES herb-acupuncture, compared to those of PD98509 and berberine. To evaluate ES herb-acupuncture as a novel anti-arthritic therapy, a polyarthritic rat model was developed using heat-killed <I>Mycobacterium tuberculosis</I>, and 50 μl of ES distillate was subcutaneously injected into the ST36 acupoint on each knee joint. While the articular indexes of arthritic rats were evidently decreased by ES herb-acupuncture, their body weights did not regain their initial levels. This may be due to the accelerating effects of ES on weight-loss and fat consumption. The mRNA expressions of TNF-α and interleukin (IL)-6 genes, which were closely stimulated in the arthritic rat joints, were found to be restored to the normal levels through the ES treatment. In the case of IL-1β, the recovery was not significant but substantial. The anti-arthritic effect of ES herb-acupuncture was not found in the ES-treated/non-acupoint group. In conclusion, the ES herb-acupuncture into the ST36 acupoint was found to be effective in alleviating the inflammatory response and thus arthritic symptoms in adjuvant-induced arthritic rats.</P>
Alteration in Metabolism and Toxicity of Acetaminophen Upon Repeated Administration in Rats
Kim, Sun J.,Lee, Min Y.,Kwon, Do Y.,Kim, Sung Y.,Kim, Young C. The Japanese Pharmacological Society 2009 JOURNAL OF PHARMACOLOGICAL SCIENCES Vol.111 No.2
<P>Our previous studies showed that administration of a subtoxic dose of acetaminophen (APAP) to female rats increased generation of carbon monoxide from dichloromethane, a metabolic reaction catalyzed mainly by cytochrome P450 (CYP) 2E1. In this study we examined the changes in metabolism and toxicity of APAP upon repeated administration. An intraperitoneal dose of APAP (500 mg/kg) alone did not increase aspartate aminotransferase, alanine aminotransferase, or sorbitol dehydrogenase activity in serum, but was significantly hepatotoxic when the rats had been pretreated with an identical dose of APAP 18 h earlier. The concentrations and disappearance of APAP and its metabolites in plasma were monitored for 8 h after the treatment. APAP pretreatment reduced the elevation of APAP-sulfate, but increased APAP-cysteine concentrations in plasma. APAP or APAP-glucuronide concentrations were not altered. Administration of a single dose of APAP 18 h before sacrifice increased microsomal CYP activities measured with <I>p</I>-nitrophenol, <I>p</I>-nitroanisole, and aminopyrine as probes. Expression of CYP2E1, CYP3A, and CYP1A proteins in the liver was also elevated significantly. The results suggest that administration of APAP at a subtoxic dose may result in an induction of hepatic CYP enzymes, thereby altering metabolism and toxicological consequences of various chemical substances that are substrates for the same enzyme system.</P>
Protective Effects of Isoliquiritigenin Against Methamphetamine-Induced Neurotoxicity in Mice
Lee, Min Jung,Yang, Chae Ha,Jeon, Jae-Pil,Hwang, Meeyul The Japanese Pharmacological Society 2009 JOURNAL OF PHARMACOLOGICAL SCIENCES Vol.111 No.2
<P>Isoliquiritigenin (ISL) suppresses cocaine-induced extracellular dopamine levels and has a neuroprotective effect in cocaine-treated rat brain. Here, we examine the effect of ISL on methamphetamine-induced striatal neurotoxicity. Repeated injections of methamphetamine cause the loss of striatal dopamine transporter (DAT) and tyrosine hydroxylase (TH). Intraperitoneal injection of ISL prior to methamphetamine injection significantly prevented methamphetamine-induced reduction of DAT and TH. ISL also suppressed methamphetamine-induced activation of glial cells. Moreover, ISL impeded the expression of nitric oxide synthase and the activation of NF-κB through blockage of its phosphorylation. Our results suggest that ISL protects against methamphetamine-induced neurotoxicity by inhibition of NF-κB activation.</P>
Kim, Young-Sick,Chang, Hyun-Kyung,Lee, Jin-Woo,Sung, Yun-Hee,Kim, Sung-Eun,Shin, Mal-Soon,Yi, Jae-Woo,Park, Je-Hoon,Kim, Hong,Kim, Chang-Ju The Japanese Pharmacological Society 2009 JOURNAL OF PHARMACOLOGICAL SCIENCES Vol.109 No.1
<P>Gabapentin was developed as an anticonvulsant, but has also been used to alleviate hyperalgesia in neuropathic pain. In this study, the protective effect of gabapentin against <I>N</I>-methyl-<SMALL>D</SMALL>-aspartate (NMDA)-induced excitotoxicity in rat hippocampal CA1 neurons was investigated. Pre-treatment with gabapentin reduced the degree of neuronal damage induced by NMDA exposure in cultured hippocampal slices. Patch-clamp studies revealed that gabapentin significantly inhibited the NMDA receptor–activated ion current in dissociated hippocampal CA1 neurons, resulting in suppression of glutamate-induced neuronal injury. These results show that gabapentin may exert protective effects against glutamate-induced neuronal injury at least in part by inhibiting the NMDA receptor–activated ion current.</P>
Park, Won Sun,Ko, Jae-Hong,Ko, Eun A,Son, Youn Kyoung,Hong, Da Hye,Jung, In Duk,Park, Yeong-Min,Choi, Tae-Hoon,Kim, Nari,Han, Jin The Japanese Pharmacological Society 2010 JOURNAL OF PHARMACOLOGICAL SCIENCES Vol.112 No.1
<P>We investigated the effects of YC-1, an activator of soluble guanylyl cyclase (sGC), on voltage-dependent K<SUP>+</SUP> (Kv) channels in smooth muscle cells from freshly isolated rabbit coronary arteries by using the whole-cell patch clamp technique. YC-1 inhibited the Kv current in a dose-dependent fashion with an apparent <I>K</I><SUB>d</SUB> of 9.67 <I>μ</I>M. It accelerated the decay rate of Kv channel inactivation without altering the kinetics of current activation. The rate constants of association and dissociation for YC-1 were 0.36 ± 0.01 <I>μ</I>M<SUP>−1</SUP>·s<SUP>−1</SUP> and 3.44 ± 0.22 s<SUP>−1</SUP>, respectively. YC-1 did not have a significant effect on the steady-state activation and inactivation curves. The recovery time constant from inactivation was decreased in the presence of YC-1, and application of train pulses (1 or 2 Hz) caused a progressive increase in the YC-1 blockade, indicating that YC-1–induced inhibition of Kv currents is use-dependent. Pretreatment with Bay 41-2272 (also a sGC activator), ODQ (a sGC inhibitor), or Rp-8-Br-PET-cGMPs (a protein kinase G inhibitor) did not affect the basal Kv current and also did not significantly alter the inhibitory effect of YC-1. From these results, we suggest that YC-1 directly inhibits the Kv current independently of sGC activation and in a state-, time-, and use-dependent fashion.</P>