• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.31-32
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• 2001

A wide array of phenolic substances, particularly those present in dietary and medicinal plants, have been reported to possess substantial anticarcinogenic and antimutagenic activities. The majority of naturally occurring phenolics retain antioxidative and anti-inflammatory properties which appear to contribute to their chemopreventive or chemoprotective activity. Inducible cyclooxygenase (COX-2) and nitric oxide synthase (iNOS) are important enzymes that mediate inflammatory processes.(omitted)

• Journal of Acupuncture Research
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• v.22 no.2
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• pp.111-121
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• 2005

Human placental extract (HPE), which is prepared from the placenta of healthy pregnant females, has been widely used in clinical field. HPE is known to possess anti-inflammatory, anti-viral, anti-oxidative, anti-mutagenic, and analgesic properties. In this study, the effect of HPE against lipopolysaccharide (LPS)-induced inflammation was investigated. From the present results, HPE was shown to suppress prostaglandin E2 synthesis (PGE2) and nitric oxide (NO) production by inhibition on the LPS-stimulated enhancement of the cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions in mouse BV2 microglial cells. These results suggest that HPE may offer a valuable mean of therapy for the treatment of brain inflammatory diseases by attenuating LPS-induced PGE2 and NO production.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.5
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• pp.1315-1321
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• 2008

Chan-Su (Venenum bufonis) has long been for a variety of other purposes including treatment of inflammation in the folk medicine recipe. Since nitric oxide (NO) is one of the major inflammatory parameters, we first studied the effects of Chan-Su on NO production in lipopolysaccharide (LPS)-stimulated BV2 microglial cells, Chan-Su inhibited the secretion of NO in BV2 microglial cells, without affecting cell viability, The protein level of inducible nitric oxide synthase (iNOS) was decreased by Chan-Su, And Chan-Su also inhibited production of prostaglandin E2 (PGE2) and expression of cyclooxygenase (COX)-2. Proinflammatory cytokines, such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$ and IL-12, were inhibited by Chan-Su in a dose-dependent manner. And Chan-Su inhibited the degradation of ${IkB-\alpha}$, which was considered to be inhibitor of nuclear factor $(NF)-{\kappa}B$, one of a potential transcription factor for the expression of iNOS, COX-2 and proinflammatory cytokines. These results suggest that Chan-Su could exert its anti-inflammatory actions by suppressing the synthesis of NO through inhibition of $I{\kappa}B-{\alpha}$ degradation.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.4
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• pp.239-246
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• 2003

The expression of cyclooxygenase-2 (COX-2) is a characteristic response to inflammation and can be inhibited with sodium salicylate. $TNF-{\alpha}$ plus $IFN-{\gamma}$ can induce extracellular signal-regulated kinase (ERK), IKK, $I{\kappa}B$ degradation and NF-${\kappa}B$ activation. The inhibition of the ERK pathway with selective inhibitor, PD098059, blocked cytokine-induced COX-2 expression and $PGE_2$ release. Salicylate treatment inhibited COX-2 expression induced by $TNF-{\alpha}$/$IFN-{\gamma}$ and regulated the activation of ERK, IKK and $I{\kappa}B$ degradation and subsequent NF-${\kappa}B$ activation in MC3T3E1 osteoblasts. Furthermore, antioxidants such as catalase, N-acetyl-cysteine or reduced glutathione attenuated COX-2 expression in combined cytokines-treated cells, and also inhibited the activation of ERK, IKK and NF-${\kappa}B$ in MC3T3E1 osteoblasts. In addition, $TNF-{\alpha}$/$IFN-{\gamma}$ stimulated ROS release in the osteoblasts. However, salicylate had no obvious effect on ROS release in DCFDA assay. The results showed that salicylate inhibited the activation of ERK and IKK, $I{\kappa}B$ degradation and NF-${\kappa}B$ activation independent of ROS release and suggested that salicylate exerts its anti-inflammatory action in part through inhibition of ERK, IKK, $I{\kappa}B$, $NF-{\kappa}B$ and resultant COX-2 expression pathway.

• Journal of Acupuncture Research
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• v.28 no.4
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• pp.19-35
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• 2011

Objectives : This study was designed to investigate the effects of acupuncturing $PC_8$ used perpendicular needling method determine the mechanism of action of acupuncturing $PC_8$ by measuring the changes of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) in normal rats. Methods : This study also investigated the effects of acupuncturing $PC_8$ on the change of rCBF in cerebral ischemic rats, and revealed the mechanism of its action. In addition, the effects of acupuncturing $PC_8$ on focal ischemic brain injury was studied in cerebral ischemic rats. Results : 1. Acupuncturing $PC_8$ significantly increase rCBF but decreased MABP in normal rats. 2. Acupuncturing $PC_8$ increased of rCBF was significantly inhibited by pretreatment with indomethacin (1mg/kg, i.p.), an inhibitor of cyclooxygenase in normal rats. 3. Acupuncturing $PC_8$ increased of rCBF was significantly inhibited by pretreatment methylene blue (10 ${\mu}g$/kg, i.p.), an inhibitor of guanylate cyclase in normal rats. 4. Acupuncturing $PC_8$ was significantly improved the rCBF than control group increased unstable in cerebral ischemic rats. 5. Acupuncturing $PC_8$ was not significantly improved the rCBF than control group by pretreatment with indomethacin (1mg/kg, i.p.), an inhibitor of cyclooxygenase in cerebral ischemic rats. 6. Acupuncturing $PC_8$ was significantly increased the rCBF than control group by pretreatment methylene blue ($10{\mu}g$/kg, i.p.), an inhibitor of guanylate cyclase in cerebral ischemic rats. Conclusions : In conclusion, our study suggested that acupuncturing $PC_8$ can increase rCBF in normal state, and improve stability of rCBF in ischemic state. In addition, we suggested that mechanisms related with acupuncturing $PC_8$ was involved in the guanylate cyclase pathway.

• Korean Journal of Acupuncture
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• v.20 no.4
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• pp.31-40
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• 2003

Objectives : The purpose of this study is to investigate whether Haenggan(LR2) Reduction in Acupuncture affects cerebral hemodynamics〔regional cerebral blood flow(rCBF), mean arterial blood pressure(MABP)〕in normal rats, and to make manifest whether Haenggan(LR2) Reduction in Acupuncture is mediated by cyclooxygenase or guanylate cyclase. Methods : This experiments was to investigate at the other changes of rCBF and MABP at Haenggan(LR2) Reduction in Acupuncture in normal rats, pretreated rats with indomethacin(1 mg/kg, i.v.) and pretreated rats with methylene blue$(10\;{\,u}g/kg,\;i.v.)$. Results : 1. Haenggan(LR2) Reduction in Acupuncture was significantly increased rCBF during acupuncture and after withdrawing of the needle. 2. Haenggan(LR2) Reduction in Acupuncture was decreased MABP during acupuncture, but Haenggan(LR2) Reduction in Acupuncture was increased MABP in compared with normal condition. 3. Pretreatment with indomethacin(1 mg/kg, i.v.) was significantly inhibited Haenggan(LR2) Reduction in Acupuncture induced increase of rCBF, but was increased Haenggan(LR2) Reduction in Acupuncture induced increase of MABP. 4. Pretreatment with methylene blue$(10\;{\mu}g/kg,\;i.v.)$ was significantly decreased Haenggan(LR2) Reduction in Acupuncture induced increase of rCBF and MABP. This results suggest that Haenggan(LR2) Reduction in Acupuncture increased rCBF by dilating pial arterial diameter, and the mechanism of Haenggan(LR2) Reduction in Acupuncture is mediated by guanylate cyclase.

• Journal of Korean Medicine Rehabilitation
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• v.20 no.3
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• pp.1-11
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• 2010

Objectives : This study was designed to investigate the effects of Lumbricus extract(LE) on the regional cerebral blood flow(rCBF) in ischemic rats, further to determine the mechanism of action of LE, and the effects that LE inhibits lactate dehydrogenase(LDH) activity in brain cells. Methods and materials : This study, ischemic rats were divided into total four group: control group(n=6), experimental group I (LE treated group)(n=6), experimental group II(LE treated group after pretreatment with indomethacin)(n=6), experimental group III(LE treated group after pretreatment with methylene blue)(n=6). And the measurement that LE inhibits LDH activity in the damage to brain cells to N-methyl-D-aspartic acid(NMDA). The changes of rCBF were determinated by laser-doppler flowmetry(LDF), and LDH activity was determinated by microplate reader in vitro. Results : 1. The rCBF was significantly improved by LE(10 mg/kg, i.p.) during the period of cerebral reperfusion, compared with the control group. 2. The rCBF was significantly increased by LE after pretreatment with indomethacin(1 mg/kg, i.p.), an inhibitor of cyclooxygenase, during the period of cerebral reperfusion, compared with the LE group, and rCBF was accelerated by LE after pretreatment with methylene blue($10{\mu}g/kg$, i.p.) an inhibitor of guanylate cyclase during the period of cerebral reperfusion, compared with the control group. 3. LE significantly inhibited LDH activity in vitro in a dose-dependent manner. Conclusions : From the above results, these were suggested that Lumbricus had anti-ischemia action in connection with cyclooxygenase and might prevent the brain cells death through inhibited LDH activity.

• Journal of Society of Preventive Korean Medicine
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• v.19 no.3
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• pp.155-170
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• 2015

Objective : Jaeumgeonbitang have been used in Korean medicine for many centuries as a therapuetic agent of vertigo. JAE was extract of Jaeumgeonbitang adding Evodiae Fructus. The effects of JAE on the cerebral blood flow and blood pressure is not known. This study was designed to investigate the effects of JAE on the ischemic crebral injuries. Method : We performed to investigate effects of JAE on the changes of regional cerebral blood flow(rCBF) and mean arterial blood pressure (MABP) in normal and ischemic rats, and further to determine the mechanism and cytokines production ($IL-1{\beta}$, $TNF-{\alpha}$, IL-10, $TGF-{\beta}$) of JAE. Results : In normal rats, JAE significantly increased rCBF and significantly decreased MABP in a dose-dependent manner. This result suggested that JAE significantly increased rCBF by dilating pial arterial diameter. Increase of JAE-induced rCBF was significantly inhibited by the pretreatment with indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase, and was significantly inhibited by methylene blue ($10{\mu}g/kg$, i.p.), an inhibitor of guanylate cyclase. Decrease of JAE-induced MABP was significantly increased by the pretreatment with indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase. So, these results suggested that the mechanism of JAE was mediated by cyclooxygenase. In ischemic rat, the rCBF was significantly and stably increased by JAE (10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in Control group. In cytokine production of serum by drawing from femoral arterial blood at 1 hr after reperfusion, Sample group (JAE 10 mg/kg treated group) was significantly decreased $IL-1{\beta}$ and $TNF-{\alpha}$ production compared with Control group. In cytokine production of serum by drawing from femoral arterial blood at 1 hr after reperfusion, Sample group was significantly increased IL-10 production compared with Control group. Conclusion : These results suggested that JAE was significantly and stably increased regional cerebral blood flow by inhibited $IL-1{\beta}$ and $TNF-{\alpha}$ production, and increased IL-10 production.

• Journal of Life Science
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• v.23 no.1
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• pp.55-62
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• 2013

The objective of this study was to evaluate the anti-inflammation effect of extract of Carthamus tinctorious seed, on skin obtained from Gyeong buk, Korea. Regulatory mechanisms of cytokines and nitric oxide (NO) involved in immunological activity of Raw 264.7 cells. Tested cells were pretreated with 70% ethanol extracted of Carthamus tinctorious seed and further cultured for an appropriated time after the addition of lipopolyssacharide (LPS). During the entire experimental period, 5, 10, 25 and 50 ${\mu}g/ml$ of Carthamus tinctorious seed showed no cytotoxicity. In these concentrations, ethyl acetate layer of ethanol extracted Carthamus tinctorius seed (CT-E/E) inhibited the production of NO and prostaglandin $E_2$ ($PGE_2$), tumor necorsis factor-a (TNF-${\alpha}$), interleukin-$1{\beta}$ (IL-$1{\beta}$), interleukin-6 (IL-6) expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2). At a 50 ${\mu}g/ml$ level of CT-E/E, $PGE_2$, iNOS and COX-2 inhibition activity were shown 60%, 38%, and 42%, respectively. In addition, CT-E/E reduced the release of inflammatory cytokines including TNF-${\alpha}$, IL-$1{\beta}$ and IL-6. These results suggest that Carthamus tinctorious seed extracts may be a potential anti-inflammatory therapeutic agent due to the significant effects on inflammatory factors.

• Journal of Life Science
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• v.22 no.9
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• pp.1137-1144
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• 2012

Inflammation is a host defense mechanism that is activated in response to harmful substances or pathogens. However, an excessive inflammatory response is a problem in itself. Macrophages secrete inflammatory mediators such as nitric oxide (NO) or cytokines through various pathways such as the nuclear factor kappa B (NF-${\kappa}B$)-activated pathway after recognizing pathogen-like lipopolysaccharides (LPSs). In this study, anti-inflammatory effects of Eupatorium chinensis var. simplicifolium (EUC) extracts were investigated using LPS-stimulated RAW 264.7 macrophages. The EUC root extract significantly reduced NO production, inducible nitric oxide synthase (iNOS) expression, and cyclooxygenase-2 expression in a concentration-dependent manner. In addition, the EUC root extract reduced phosphorylation of mitogen-activated protein kinases and protein kinase B, which is upstream of NF-${\kappa}B$. The EUC root extract also reduced the degradation of inhibitory kappa B. These results indicate that EUC root extract exerts anti-inflammatory effects, which are mediated by inhibition of iNOS expression and the NF-${\kappa}B$ pathway.