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Lee Y.-S.,Dong - Eui University | Lee J.-H.,Chemistry and Biotechnology Examination Bureau | Lee I.-S.,Dong - Eui University | Choi B.-T.,Pusan National University
Molecular Medicine Reports

The effects of electroacupuncture (EA) on spinal α-amino-3-hydroxy-5- methyl-4-isoxazole-propionic acid (AMPA) receptor subunits in male rats injected with complete Freund's adjuvant (CFA) were investigated. Bilateral EA stimulation (2 Hz, 1 mA) was administered by needle insertion for 30 min once daily at acupoints corresponding to Zusanli and Sanyinjiao, and the thermal thresholds were measured. To examine the changes in the AMPA receptor subunits, the L4-5 segments of the spinal cord were analyzed by qPCR, western blot analysis and immunohistochemistry. The CFA-induced thermal sensitivity of the rat hind paw was significantly inhibited by EA stimulation from day 3 following CFA injection. On day 5 following CFA injection, there were no significant changes in the expression of the AMPA receptor GluR1 subunit in the CFA-injected rats with or without EA stimulation, compared with the control rats. However, the expression of the GluR2 subunit was significantly decreased by CFA treatment. Western blot analysis revealed that the expression of the phosphorylated GluR1 subunit in the control rats was not significantly different compared with that in the CFA-injected rats with and without EA stimulation. However, phosphorylation of the ipsilateral GluR2 subunit was significantly increased in the CFA-injected rats, and this activation was prevented by EA stimulation. Immunohistochemical analysis revealed a greater expression of phospho-GluR2 following CFA injection, which was inhibited by EA stimulation. These results suggested that phosphorylation of the AMPA receptor, particularly the GluR2 subunit, may be important in EA analgesia of CFA-induced inflammation. Source

Shin D.Y.,Dongnam Institute of Radiological and Medicine science | Kim G.-Y.,Jeju National University | Lee J.H.,Chemistry and Biotechnology Examination Bureau | Choi B.T.,Pusan National University | And 2 more authors.
International Journal of Molecular Sciences

Diallyl disulfide (DADS), a sulfur compound derived from garlic, has various biological properties, such as anticancer, antiangiogenic and anti-inflammatory effects. However, the mechanisms of action underlying the compound's anticancer activity have not been fully elucidated. In this study, the apoptotic effects of DADS were investigated in DU145 human prostate carcinoma cells. Our results showed that DADS markedly inhibited the growth of the DU145 cells by induction of apoptosis. Apoptosis was accompanied by modulation of Bcl-2 and inhibitor of apoptosis protein (IAP) family proteins, depolarization of the mitochondrial membrane potential (MMP, ΔΨm) and proteolytic activation of caspases. We also found that the expression of death-receptor 4 (DR4) and Fas ligand (FasL) proteins was increased and that the level of intact Bid proteins was down-regulated by DADS. Moreover, treatment with DADS induced phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular-signal regulating kinase (ERK), p38 MAPK and c-Jun N-terminal kinase (JNK). A specific JNK inhibitor, SP600125, significantly blocked DADS-induced-apoptosis, whereas inhibitors of the ERK (PD98059) and p38 MAPK (SB203580) had no effect. The induction of apoptosis was also accompanied by inactivation of phosphatidylinositol 3-kinase (PI3K)/Akt and the PI3K inhibitor LY29004 significantly increased DADS-induced cell death. These findings provide evidence demonstrating that the proapoptotic effect of DADS is mediated through the activation of JNK and the inhibition of the PI3K/Akt signaling pathway in DU145 cells. © 2012 by the authors; licensee MDPI, Basel, Switzerland. Source

Lee S.H.,Korea Advanced Institute of Science and Technology | Lee J.H.,Chemistry and Biotechnology Examination Bureau | Oh E.Y.,Meridian | Kim G.-Y.,Jeju National University | And 4 more authors.
International Journal of Molecular Medicine

Chronic microglial activation endangers neuronal survival through the release of various toxic pro-inflammatory molecules; thus, negative regulators of microglial activation have been identified as potential therapeutic candidates for several neurological diseases. In this study, we investigated the inhibitory effects of an ethanol extract of Cnidium officinale rhizomes (EECO), which has been used as a herbal drug in Oriental medicine, on the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators, such as nitric oxide (NO) and prostaglandin E2 (PGE2), as well as that of pro-inflammatory cytokines in BV2 microglia cells. EECO significantly inhibited the excess production of NO and PGE2 in LPS-stimulated BV2 microglia cells. It also attenuated the expression of inducible NO synthase, cyclooxygenase-2, as well as that of pro-inflammatory cytokines, such as interleukin-1β and tumor necrosis factor-α. Moreover, EECO exhibited anti-inflammatory properties by suppressing nuclear factor-κB (NF-κB) translocation and the activation of the phosphoinositide 3-kinase/Akt pathway in LPS-stimulated BV2 cells. These results indicate that EECO exerts anti-inflammatory effects in LPS-stimulated BV2 microglial cells by inhibiting pro-inflammatory mediators and cytokine production by blocking the NF-κB pathway. These findings suggest that EECO has substantial therapeutic potential for the treatment of neurodegenerative diseases accompanied by microglial activation. Source

Choi E.-A.,SALt Inc | Park C.,Korea University | Han M.-H.,Korea University | Lee J.H.,Chemistry and Biotechnology Examination Bureau | And 3 more authors.
Experimental and Therapeutic Medicine

Sarijang is a bamboo salt soy sauce, containing extracts of Rhynchosia nulubilis, sulfur-fed duck, dried bark of Ulmus davidiana and Allium sativum, which has been demonstrated to exert anti-inflammatory and antitumor activity. However, the cellular and molecular mechanisms of action of sarijang have not yet been elucidated. In the present study, we investigated the pro-apoptotic effects of sarijang in an in vitro U937 human leukemia cell model. Treatment with sarijang resulted in a concentration-dependent growth inhibition of the cells, coupled with the characteristic morphological features of apoptosis. The induction of the apoptotic cell death of the U937 cells by sarijang exhibited a correlation with the upregulation of death receptor 4 (DR4), the downregulation of members of the inhibitor of apoptosis protein (IAP) family, including survivin and cellular IAP (cIAP)-1, and the cleavage of Bid. Apoptosis-inducing concentrations of sarijang also induced the activation of caspases (caspase-3, -8 and -9), accompanied by proteolytic degradation of poly(ADP-ribose)-polymerase, β-catenin and phospholipase C-γ1. However, the apoptosis induced by sarijang was significantly inhibited by z-VED-fmk, a pan-caspase inhibitor, which demonstrated the importance of caspases in the process. These results suggested that sarijang may be a potential chemotherapeutic agent for use in the control of U937 human leukemia cells. Further studies are required to identify the active compounds in sarijang. Source

Kim Y.R.,Pusan National University | Kim H.N.,Pusan National University | Jang J.Y.,Pusan National University | Park C.,Korea University | And 4 more authors.
International Journal of Molecular Medicine

In this study, we investigated the molecular mechanisms underlying the anti-apoptotic properties of electroacupuncture (EA) in a rat model of middle cerebral artery occlusion (MCAO). Treatment with 2 Hz EA (1 mA) resulted in a markedly reduced infarct area after stroke, particularly in the middle region of the brain. Treatment with EA resulted in a significant decrease in the number of apoptotic cells identified by Hoechst 33342 and TUNEL staining. According to the results of the analysis for proteins involved in apoptosis, treatment with EA resulted in a significantly reduced expression of death receptor (DR)5. Among the members of the Bcl-2 family, a higher expression of anti-apoptotic Bcl-2 and Bcl-xL was observed in the rats treated with EA, compared with the untreated rats with MCAO. As regards the expression of the inhibitor of apoptosis protein (IAP) family, a higher expression of anti-apoptotic cIAP-1 and -2 was also detected in the cortex of the EA-treated rats. Using western blot analysis, we observed that activated caspase-3 was only significantly arrested by EA treatment in the rats with MCAO; however, according to the results of the caspase assay, the activities of caspase-3, -8 and -9 were markedly inhibited by EA treatment. These results suggest that treatment with EA exerts anti apoptotic effects in cerebral ischemia in a rat model of MCAO and that these effects are associated with the inhibition of the DR and mitochondrial apoptotic pathways. Source

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