• Journal of Physiology & Pathology in Korean Medicine
• /
• v.20 no.6
• /
• pp.1612-1619
• /
• 2006

This Study was designed to investigate the mechanism of Mixture of Bambusae Caulis in Liquamen and Bamboo Extract on the change of regional cerebral blood flow (rCBF) and blood pressure (BP) in normal rats, and further to investigate cytokines production in serum of cerebral ischemic rats. Mixture were as follows ; Bamboo Extract extracted with distilled water at 98 $^{\circ}C$ for 3 hrs, Mixture of Bambusae Caulis in Liquamen and bamboo Extracts (MLE) mixed at the ratio 1 to 100 (MLE100), 1 to 50 (MLE50), 1 to 20 (MLE20), 1 to 10 (MLE10), 1 to 5 (MLE5). The results were as follows ; The MLE-induced increase in rCBF was significantly inhibited by pretreatment with indomethacin (1 mg/kg, I.p.), an inhibitor of cyclooxygenase as well as methylene blue (10 $^{\mu}g/kg$, I.p.), an inhibitor of guanylate cyclase. The MLE-induced increase in BP was significantly inhibited by pretreatment with methylene blue. In cytokines production in the serum drawn from femoral arterial 1 hr after middle cerebral artery occlusion, MLE5 significantly increased production of TGF-${\beta}$ and increased production of IL-10, but significantly decreased production of TGF-${\alpha}$ compared with control group. In cytokines production in the serum drawn from femoral arterial 1 hr after reperfusion, MLE5 significantly increased production of TGF-${\beta}$ and IL-10, but significantly decreased production of TGF-${\alpha}$ compared with control group. AS results above. And MLE5 had anti-ischemic effect by inhibiting TGF-${\alpha}$ production, and by accelerating IL-10 and TGF-${\beta}$ production.

• Herbal Formula Science
• /
• v.13 no.1
• /
• pp.49-69
• /
• 2005

This Study was designed to investigate the effect of Sunkihwalhyul -Tang extract(SHT) on the change of cerebral hemodynamics [regional cerebral blood flow(rCBF), pial arterial diameter(PAD) and mean arterial blood pressure(MABP)] in normal and cerebral ischemic rats, and further to determine the mechanisms of action of SHT on hemodynamics. In addition, this study was designed to investigate whether SHT inhibits lactate dehydrog enase(LDH) activity in neuronal cells and cytokines production in serum of cerebral ischemic rats. The results were as follows 1. SHT significantly increased rCBF and PAD in a dose-dependent manner, but MABP was not changed by injecting SHT. These results suggest that SHT significantly increases rCBF by dilating PAD. 2. The SHT-induced increase in rCBF was significantly inhibited by pretreatment with indomethacin(IDN, 1 mg/kg, i.p.), an inhibitor of cyclooxygenase and methylene blue(MTB, $10{\mu}g/kg$, i.p.), an inhibitor of guanylate cyclase. 3. The SHT-induced dilation in PAD was significantly inhibited by pretreatment with IDN and MTB. 4. The SHT-induced some increase in MABP was significantly increased by pretreatment with IDN. These results suggest that the mechanism of action of SBT is mediated by guanylate cyclase. 5. Both rCBF and PAD were significantly and stably increased by SHT(10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. 6. SBH significantly inhibited LDH activity in neuronal cells. These results suggest that SHT prevents the neuronal death. 7. In cytokine production in the senlm drawn from femoral artery 1 hr after middlecerebral arterial occlusion, sample group showed significantly decreased production of IL-1$\beta$ production, decreased production TNF-$\alpha$ and increased Production of IL-10 compared with control group. 8. In cytokine production in the serum drawn femoral artery 1 hr after reperfusion, sample group showed significantly decreased production of IL-1$\beta$ and TNF-$\alpha$ as wellas significantly increased production of IL10 compared with control group. These results suggest that SHT mediated by guanylate cyclase has inhibitive effect on the brain damage by inhibiting LDH activity, IL-1$\beta$ and TNF-$\alpha$ production, and by accelerating IL-10 production. The present author thinks that SHT has an anti-ischemic effects through the improvement of cerebral hemodynamics and inhibitive enects on the brain damage.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.18 no.6
• /
• pp.1714-1721
• /
• 2004

This experimental study was designed to investigate the mechanism of Palmul-Tang(PMT) on the changes of cerebral hemodynamics in rats. The changes of cerebral hemodynamics in normal rats were as follows ; The PMT-induced increase in regional cerebral blood flow was significantly inhibited by pretreatment with indomethacin(1㎎/㎏, i.p.), an inhibitor of cyclooxygenase, and was inhibited by methylene blue(10㎍/㎏, i.p.), an inhibitor of guanylate cyclase. The PMT-induced dilation in pial arterial diameter was significantly inhibited by pretreatment with indomethacin and methylene blue. The PMT-induced increase in mean arterial blood pressure was significantly inhibited by pretreatment with indomethacin but was increased by methylene blue. This results were suggested that the mechanism of PMT was mediated by cyclooxygenase. The changes of cytokine production in cerebral ischemic rats were as follows ; In cytokine production of serum by drawing from femoral arterial blood after middle cerebral arterial occlusion 1hr, sample group was decreased IL-1β and TNF-α production compared with control group, IL-10 production of sample group was similar to that of control group, but sample group was significantly increased TGF-β production compared with control group. In cytokine production of serum by drawing from femoral arterial blood after reperfusion 1hr, sample group was significantly decreased IL-1β production compared with control group and decreased TNF-α production compared with control group. IL-10 production of sample group was similar to that of control group, but sample group was significantly increased TGF-β production compared with control group. In cytokine production of serum by drawing from femoral arterial blood after reperfusion 4 hrs, sample group was significantly decreased IL-1β production compared with control group, but IL-10 production of sample group was similar to that of control group. sample group was increased TNF-α and TGF-β production compared with control group. These results suggested that PMT had inhibitive effect on the brain damage by inhibiting IL-1β and TNF-α production, but by accelerating TGF-β production. The present author thought that PMT had an anti-ischemic effect through the improvement of cerebral hemodynamics and inhibitive effect on the brain damage.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.21 no.5
• /
• pp.1127-1134
• /
• 2007

The study was designed to investigate the mechanism of Patholoobi Caulis freeze dried powder (PCF) on the regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) in normal rats and cytokines production ($IL-1{\beta}$, $TNF-{\alpha}$, IL-10, $TGF-{\beta}$) in cerebral ischemic rats. The results in normal rats were as follows ; Increase of PCF-induced rCBF was significantly inhibited by pretreatment with methylene blue (10 ${\mu}g/kg$, I.p.), an inhibitor of guanylate cyclase, and was inhibited by indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase. Increase of PCF-induced MABP was decreased by pretreatment with methylene blue, but was increased by indomethacin. These results suggested that the mechanism of action PCF was mediated by cyclic 3',5'-guanosine monophosphate. The results in cerebral ischemic rats were as follows ; In cytokine production in serum from femoral arterial blood 1 hr after middle cerebral arterial occlusion, PCF (10 mg/kg. i.p.) significantly decreased $IL-1{\beta}$ and $TNF-{\alpha}$ production, and increased IL-10 production compared with control group. In cytokine production in serum from femoral arterial blood 1 hr 1 hr after reperfusion, PCF (10 mg/kg, i.p.) significantly decreased $IL-1{\beta}$ production, and incresed IL-10 production compared with control group. These results suggested that PCF was significantly and stably increased regional cerebral blood flow by inhibiting $IL-1{\beta}$ production, and by accelerating IL-10 production.

• The Journal of Korean Medicine
• /
• v.26 no.3 s.63
• /
• pp.188-203
• /
• 2005

Objectives : This study was designed to investigate the effects of Jayun-tang extract (JYT) on the change of cerebral hemodynamics [regional cerebral blood flow (rCBF), pial arterial diameter (PAD) and mean arterial blood pressure (MABP)] in normal and cerebral ischemic rats, na to determine the mechanisms of action of JYT. Methods : We investigated whether JYT inhibits lactate dehydrogenase activity in neuronal cells and cytokines production in serum of cerebral ischemic rats. Results : 1. JYT significantly increased rCBF and PAD in a dose-dependent manner, but MABP was not changed by injecting JYT. These results suggested JYT significantly increased rCBF by dilating PAD. 2. The JYT-induced increase in rCBF was significantly inhibited from pretreatment with indomethacin (1mg/kg, i.p.), an inhibitor of cyclooxygenase and methylene blue $(10{\mu}g/kg, i.p.)$, an inhibitor of guanylate cyclase. 3. The JYT-induced dilation in PAD was significantly inhibited from pretreatment with indomethacin, but was increased by pretreatment with methylene blue. 4 The JYT-induced increase in MABP was reduced by pretreatment with indomethacin and methylene blue. 5. JYT significantly inhibited lactate dehydrogenase activity in neuronal cells. These results suggest that JYT prevented the neuronal death. 6. Both rCBF and PAD were significantly and stably increased by JYT $(10{\mu}g/kg,\;i.p.)$ during the Period or cerebral reperfusion, which contrasted with the findings of rapid and marked increase in the control group. 7. In cytokine production in the serum drawn from femoral artery 1hr after middle cerebral artery occlusion, the sample group showed significantly decreased production of $IL-1\beta$ and $TNF-\alpha$ as well as increased production of IL-10 and $TGF-\beta$ compared with rho control group. 8. In cytokine production in the serum drawn from femoral artery 1hr after reperfusion, the sample group showed significantly decreased production of $IL-1\beta$ and $TNF-\alpha$ as well as significantly increased production of IL-10 and $TGF-\beta$ compared with the control group. Conclusions : JYT mediated by cyclooxygenase had an inhibitive effect on brain damage by inhibiting lactate dehydrogenase activity, $IL-1\beta$ and $TNF-\alpha$ production, and by accelerating IL-10 and $TGF-\beta$ production. The author feels that JYT had anti-ischemic effects through the improvement of cerebral hemodynamics and inhibitive effects on brain damage.

• Journal of Society of Preventive Korean Medicine
• /
• v.19 no.3
• /
• pp.155-170
• /
• 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 Physiology & Pathology in Korean Medicine
• /
• v.18 no.6
• /
• pp.1643-1651
• /
• 2004

This experimental study was designed to investigate the effects of SIEGESBECKIAE HERBA extract (SHE) on the change of cerebral hemodynamics 〔regional cerebral blood flow (rCBF) and mean arterial blood pressure(MABP)〕 in normal condition and cerebral ischemic rats, and to determine the mechanism of action of SHE. This study was designed to investigate whether or not SHE inhibit lactate dehydrogenase (LDH) activity in neuronal cells and cytokines production in serum of cerebral ischemic rats. The results were as follows SHE increased rCBF significantly in a dose-dependent manner, but MABP was not changed by SHE in normal rats. The SHE-induced increase in rCBF was significantly inhibited by pretreatment with indomethacin (IDN), an inhibitor of cyclooxygenase but was increased by methylene blue (MTB), an inhibitor of guanylate cyclase. SHE inhibited lactate dehydrogenase (LDH) activity significantly in neuronal cells. rCBF was increased significantly and stably by SHE(10㎎/㎏, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group in ischemic rats. In serum by drawing from femoral arterial blood after middle cerebral arterial occlusion(MCAO) for 1hr and reperfusion for 1hr, the sample group was decreased IL-1β production significantly compared to that of the control group. In serum by drawing from femoral arterial blood after MCAO 1hr and reperfusion 1hr, sample group decreased TNF-α production significantly compared to that of the control grolilp. In serum by drawing from femoral arterial blood after reperfusion 1hr, sample group increased TGF-β production significantly compared to that of the control group. In serum by drawing from femoral arterial blood after MCAO for 1hr and reperfusion for 1hr, IL-10 production of the sample group was similar to that of control group. These results suggested that SHE had inhibitive effect on the brain damage by inhibited LDH activity, IL-1β and TNF-α production, but accelerated TGF-β production.

• International Journal of Oral Biology
• /
• v.34 no.1
• /
• pp.7-14
• /
• 2009

Nitric oxide (NO) acts as an intracellular messenger at the physiological level but can be cytotoxic at high concentrations. The cells within periodontal tissues, such as gingival and periodontal fibroblasts, contain nitric oxide syntheses and produce high concentrations of NO when exposed to bacterial lipopolysaccharides and cytokines. However, the cellular mechanisms underlying NO-induced cytotoxicity in periodontal tissues are unclear at present. In our current study, we examined the NO-induced cytotoxic mechanisms in human gingival fibroblasts (HGF). Cell viability and the levels of reactive oxygen species (ROS) were determined using a MTT assay and a fluorescent spectrometer, respectively. The morphological changes in the cells were examined by Diff-Quick staining. Expression of the Bcl-2 family and Fas was determined by RT-PCR or western blotting. The activity of caspase-3, -8 and -9 was assessed using a spectrophotometer. Sodium nitroprusside (SNP), a NO donor, decreased the cell viability of the HGF cells in a dose- and time-dependent manner. SNP enhanced the production of ROS, which was ameliorated by NAC, a free radical scavenger. ODQ, a soluble guanylate cyclase inhibitor, did not block the SNP-induced decrease in cell viability. SNP also caused apoptotic morphological changes, including cell shrinkage, chromatin condensation, and DNA fragmentation. The expression of Bax, a member of the proapoptotic Bcl-2 family, was upregulated in the SNP-treated HGF cells, whereas the expression of Bcl-2, a member of the anti-apoptotic Bcl-2 family, was downregulated. SNP augmented the release of cytochrome c from the mitochondria into the cytosol and enhanced the activity of caspase-8, -9, and -3. SNP also upregulated Fas, a component of the death receptor assembly. These results suggest that NO induces apoptosis in human gingival fibroblast via ROS and the Bcl-2 family through both mitochondrial- and death receptor-mediated pathways. Our data also indicate that the cyclic GMP pathway is not involved in NO-induced apoptosis.